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        <title>International Journal of Oncology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'International Journal of Oncology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=International+Journal+of+Oncology&t=International+Journal+of+Oncology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 08:41:36 +0100</lastBuildDate>
        <item>
            <title>Downregulation of heparanase by RNA interference inhibits invasion and             tumorigenesis of hepatocellular cancer cells in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5625220&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267022%26dopt%3DAbstract</link>
            <description>Downregulation of heparanase by RNA interference inhibits invasion and       tumorigenesis of hepatocellular cancer cells in vitro and in vivo.
    Int J Oncol. 2012 Jan 20;
    Authors: Xiong Z, Lü MH, Fan YH, Cao YL, Hu CJ, Wu YY, Wang SM, Luo G, Fang DC, Li C, Yang SM
    Abstract
    Heparanase is an endoglycosidase that degrades heparan sulfate, the main       polysaccharide constituent of the extracellular matrix and basement membrane.       The expression of heparanase is associated with invasion, as well as the angiogenic       and metastatic potential of diverse malignant tumors. We used RNA interference       strategies to evaluate the role of human heparanase in a liver cancer cell line       and to explore the therapeutic potential of its specific targeting. Using an online   ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625220</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Upregulated expression of ADAM12 is associated with progression of oral             squamous cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5625219&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267082%26dopt%3DAbstract</link>
            <description>This study suggests that       controlling the expression or activity of ADAM12 could be a useful strategy in       the development of an effective cure for OSCC.
    PMID: 22267082 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625219</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625219</guid>        </item>
        <item>
            <title>Blockade of TRPM8 activity reduces the invasion potential of oral squamous             carcinoma cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=5625218&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267123%26dopt%3DAbstract</link>
            <description>Blockade of TRPM8 activity reduces the invasion potential of oral squamous       carcinoma cell lines.
    Int J Oncol. 2012 Jan 20;
    Authors: Okamoto Y, Ohkubo T, Ikebe T, Yamazaki J
    Abstract
    Several members of the transient receptor potential (TRP)-channel family       are expressed in cancer cells. One, cold/menthol-sensitive TRPM8, is reportedly       an important player in carcinogenesis in human prostate cancer, although its involvement       in oral squamous cell carcinoma (SCC) remains unclear. The present immunohistochemistry       and RT-PCR results revealed intense TRPM8 expression in two SCC cell lines, HSC3       and HSC4, derived from the human tongue. Menthol, icilin, and a more specific       TRPM8 agonist (WS-12) induced non-specific cation currents, with Ca2+ p...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625218</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625218</guid>        </item>
        <item>
            <title>Identification of prognostic biomarkers for response to radiotherapy             by DNA microarray in nasopharyngeal carcinoma patients.</title>
            <link>http://www.medworm.com/index.php?rid=5625217&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22267178%26dopt%3DAbstract</link>
            <description>Identification of prognostic biomarkers for response to radiotherapy       by DNA microarray in nasopharyngeal carcinoma patients.
    Int J Oncol. 2012 Jan 20;
    Authors: Yang S, Chen J, Guo Y, Lin H, Zhang Z, Feng G, Hao Y, Cheng J, Liang P, Chen K, Wu H, Li Y
    Abstract
    Nasopharyngeal carcinoma (NPC) is a malignancy with an unusually variable       incidence rate across the world. Radiotherapy is the primary treatment modality       for NPC, but radiation resistance remains a serious obstacle to successful treatment       in many cases. To identify the genes involved in this resistance and to find molecular       markers for predicting NPC response to radiotherapy, we compare the expression       profiles of 12 radiation-resistant patient biopsy specimens and 8 radiation-sensiti...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625217</comments>
            <pubDate>Fri, 20 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625217</guid>        </item>
        <item>
            <title>Mucin production determines sensitivity to bortezomib and gemcitabine             in pancreatic cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5625221&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266985%26dopt%3DAbstract</link>
            <description>Mucin production determines sensitivity to bortezomib and gemcitabine       in pancreatic cancer cells.
    Int J Oncol. 2012 Jan 18;
    Authors: Wissniowski TT, Meister S, Hahn EG, Kalden JR, Voll R, Ocker M
    Abstract
    The prognosis of pancreatic cancer remains disappointing due to a high intrinsic       resistance against chemotherapeutic agents. Standard gemcitabine therapies have       improved overall survival only marginally and recently, inhibition of the proteasome       by the boronic acid derivative bortezomib has been introduced as a novel therapeutic       strategy for solid and hematological malignancies including pancreatic cancer.       The mucus-producing pancreatic cancer cell line Capan-1 was cultured under standard       conditions and treated with different conce...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625221</comments>
            <pubDate>Wed, 18 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625221</guid>        </item>
        <item>
            <title>Inhibition of androgen-responsive LNCaP prostate cancer cell tumor xenograft             growth by dietary phenethyl isothiocyanate correlates with decreased angiogenesis             and inhibition of cell attachment.</title>
            <link>http://www.medworm.com/index.php?rid=5625223&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266918%26dopt%3DAbstract</link>
            <description>Inhibition of androgen-responsive LNCaP prostate cancer cell tumor xenograft       growth by dietary phenethyl isothiocyanate correlates with decreased angiogenesis       and inhibition of cell attachment.
    Int J Oncol. 2012 Jan 17;
    Authors: Hudson TS, Perkins SN, Hursting SD, Young HA, Kim YS, Wang TC, Wang TT
    Abstract
    Phenethyl isothiocyanate (PEITC) is a candidate anticancer compound found       in certain cruciferous vegetables. In our tumor cell xenograft model, dietary       administration of PEITC (100-150 mg/kg body weight/d) inhibited androgen-responsive       LNCaP human prostate cancer cell tumor growth. We found that dietary treatment       with PEITC significantly inhibited tumor platelet/endothelial cell adhesion molecule       (PECAM-1/CD31) expression, a mark...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625223</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625223</guid>        </item>
        <item>
            <title>Expression analysis of Cdc42 in lung cancer and modulation of its expression             by curcumin in lung cancer cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=5625222&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266952%26dopt%3DAbstract</link>
            <description>Expression analysis of Cdc42 in lung cancer and modulation of its expression       by curcumin in lung cancer cell lines.
    Int J Oncol. 2012 Jan 17;
    Authors: Chen QY, Jiao DM, Yao QH, Yan J, Song J, Chen FY, Lu GH, Zhou JY
    Abstract
    Cdc42, a Rho GTPase family member, is involved in cell transformation, proliferation,       survival, invasion and metastasis of human cancer cells. Overexpression of Cdc42       has been reported in several types of human cancer. However, the underlying mechanisms       are not well understood. The present study showed that Cdc42 was overexpressed       in 80 of 110 primary lung cancer patients, and overexpression of Cdc42 was significantly       associated with high TNM stage and lymph node metastasis. Moreover, RNAi-mediated       suppression o...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625222</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625222</guid>        </item>
        <item>
            <title>MUC2 protein expression status is useful in assessing the effects of             hyperthermic intraperitoneal chemotherapy for peritoneal dissemination of colon             cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5625224&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22266876%26dopt%3DAbstract</link>
            <description>MUC2 protein expression status is useful in assessing the effects of       hyperthermic intraperitoneal chemotherapy for peritoneal dissemination of colon       cancer.
    Int J Oncol. 2012 Jan 16;
    Authors: Fujishima Y, Goi T, Kimura Y, Hirono Y, Katayama K, Yamaguchi A
    Abstract
    We conducted a molecular biological investigation to determine the outcomes       of hyperthermic intraperitoneal chemotherapy (HIPEC) treatment, and whether it       is effective in all cases for patients with peritoneal dissemination of colon       cancer. In the HIPEC group, the 3-year survival rate was 39.2%, whereas in the       non-HIPEC group the 3-year survival rate was 15.6%. MUC2 expression was investigated       in the HIPEC group, in patients positive for MUC2 expression, and the 3-year sur...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625224</comments>
            <pubDate>Mon, 16 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625224</guid>        </item>
        <item>
            <title>Puerarin suppresses production of nitric oxide and inducible nitric             oxide synthase in lipopolysaccharide-induced N9 microglial cells through regulating             MAPK phosphorylation, O-GlcNAcylation and NF-κB translocation.</title>
            <link>http://www.medworm.com/index.php?rid=5625227&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246431%26dopt%3DAbstract</link>
            <description>Puerarin suppresses production of nitric oxide and inducible nitric       oxide synthase in lipopolysaccharide-induced N9 microglial cells through regulating       MAPK phosphorylation, O-GlcNAcylation and NF-κB translocation.
    Int J Oncol. 2012 Jan 13;
    Authors: Zheng GM, Yu C, Yang Z
    Abstract
    Microglial cells play a critical role in mediating central nervous system       inﬂammatory processes. Activated microglial cells induced by proinflammatory factor,       such as lipopolysaccharide (LPS), release many kinds of neurotoxic cytokines including       reactive oxygen species (ROS) which contributes to the pathogenesis of neurodegenerative       diseases. Puerarin, extracted from kudzu root, possesses the characteristic of       neuroprotection, antioxidation and anticanc...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625227</comments>
            <pubDate>Fri, 13 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625227</guid>        </item>
        <item>
            <title>Inhibition of migration and invasion of LNCaP human prostate carcinoma             cells by cordycepin through inactivation of Akt.</title>
            <link>http://www.medworm.com/index.php?rid=5625226&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246470%26dopt%3DAbstract</link>
            <description>In this study, the relationship between inhibition of cell motility       and anti-invasive activity by cordycepin in LNCaP human prostate carcinoma cells       was investigated. Within the concentration range that was not cytotoxic, cordycepin       time-dependently inhibited cell motility and invasiveness of LNCaP cells. The       inhibitory effects of cordycepin on cell invasiveness were associated with tightening       of tight junctions (TJs), which was demonstrated by an increase in transepithelial       electrical resistance (TER). Immunoblotting indicated that cordycepin decreases       levels of claudin proteins, which are major components of TJs that play a key       role in control and selectivity of paracellular transport. Furthermore, cordycepin       inhibited the expression ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625226</comments>
            <pubDate>Fri, 13 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625226</guid>        </item>
        <item>
            <title>Nestin as a novel therapeutic target for pancreatic cancer via tumor             angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5625225&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246533%26dopt%3DAbstract</link>
            <description>In conclusion, nestin was expressed in small proliferating       blood vessels in pancreatic cancer tissues and may be a useful marker of angiogenesis       in pancreatic ductal adenocarcinoma tissues. Furthermore, nestin is a potential       novel therapeutic target in pancreatic cancers to inhibit tumor angiogenesis.
    PMID: 22246533 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625225</comments>
            <pubDate>Fri, 13 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625225</guid>        </item>
        <item>
            <title>Millimeter wave treatment induces apoptosis via activation of the mitochondrial-dependent             pathway in human osteosarcoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5625228&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246399%26dopt%3DAbstract</link>
            <description>Millimeter wave treatment induces apoptosis via activation of the mitochondrial-dependent       pathway in human osteosarcoma cells.
    Int J Oncol. 2012 Jan 12;
    Authors: Wu G, Chen X, Peng J, Cai Q, Ye J, Xu H, Zheng C, Li X, Ye H, Liu X
    Abstract
    Millimeter wave (MW) is an electromagnetic wave with a wavelength between       1 and 10 mm and a frequency of 30-300 GHz that causes multiple biological effects       and has been used as a major component in physiotherapies for the clinical treatment       of various types of diseases including cancers. However, the precise molecular       mechanism of the anticancer activity of millimeter wave remains to be elucidated.       In the present study, we investigated the cellular effects of the MW in the U-2OS       human osteosarcoma ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625228</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625228</guid>        </item>
        <item>
            <title>Change in gene expression profiles of secreted frizzled-related proteins             (SFRPs) by sodium butyrate in gastric cancers: Induction of promoter demethylation             and histone modification causing inhibition of Wnt signaling.</title>
            <link>http://www.medworm.com/index.php?rid=5625231&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246241%26dopt%3DAbstract</link>
            <description>Change in gene expression profiles of secreted frizzled-related proteins       (SFRPs) by sodium butyrate in gastric cancers: Induction of promoter demethylation       and histone modification causing inhibition of Wnt signaling.
    Int J Oncol. 2012 Jan 10;
    Authors: Shin H, Kim JH, Lee YS, Lee YC
    Abstract
    Activation of Wnt signaling without mutation of β-catenin or APC occurs       frequently in human gastric cancers. Secreted frizzled-related protein (SFRP),       a negative modulator of the Wnt signaling pathway, are frequently inactivated       in human gastric cancers. Inhibition of SFRP gene expression may account for the       Wnt/β-catenin activation in human gastric cancer. However, the molecular mechanisms       of silencing of SFRP genes are not fully understood. ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625231</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625231</guid>        </item>
        <item>
            <title>Heat shock protein 90 is a promising target for effective growth inhibition             of gastrointestinal neuroendocrine tumors.</title>
            <link>http://www.medworm.com/index.php?rid=5625230&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246317%26dopt%3DAbstract</link>
            <description>In conclusion, this study showed that Hsp90 inhibition may be an attractive       target for innovative GEP-NET treatment alone or in combination with either IGF-1R       or mTOR inhibitors.
    PMID: 22246317 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625230</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625230</guid>        </item>
        <item>
            <title>Blockade of irradiation-induced autophagosome formation impairs proliferation             but does not enhance cell death in HCT-116 human colorectal carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5625229&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22246348%26dopt%3DAbstract</link>
            <description>Blockade of irradiation-induced autophagosome formation impairs proliferation       but does not enhance cell death in HCT-116 human colorectal carcinoma cells.
    Int J Oncol. 2012 Jan 10;
    Authors: de Albuquerque-Xavier AC, Bastos LG, de Freitas JC, Leve F, de Souza WF, de Araujo WM, Wanderley JL, Tanaka MN, de Souza W, Morgado-Díaz JA
    Abstract
    This work was undertaken to gain further information on the molecular mechanisms       underlying autophagosome formation and its relation with tumor cell survival in       response to radiation in colon cancer. A human colon cancer cell line, HCT-116,       was examined with respect to cell survival after blockade of irradiation-induced       autophagosome formation by pharmacological interference. Autophagosome formation       was c...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625229</comments>
            <pubDate>Tue, 10 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625229</guid>        </item>
        <item>
            <title>Low circulating serum levels of second mitochondria-derived activator             of caspase (Smac/DIABLO) in patients with bladder cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5579184&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22218530%26dopt%3DAbstract</link>
            <description>Low circulating serum levels of second mitochondria-derived activator       of caspase (Smac/DIABLO) in patients with bladder cancer.
    Int J Oncol. 2012 Jan 3;
    Authors: Mizutani Y, Katsuoka Y, Bonavida B
    Abstract
    Smac/DIABLO promotes apoptosis by antagonizing inhibitor of apoptosis proteins.       The expression of Smac/DIABLO in tissues has been reported in various cancers;       however, little is known about circulating levels of Smac/DIABLO. The present       study was designed to first determine if Smac/DIABLO can be detected in the serum       and then assess whether the circulating levels of Smac/DIABLO are of prognostic       significance in patients with bladder cancer. The levels of Smac/DIABLO in the       sera of 173 patients with bladder cancer and 36 normal don...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579184</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579184</guid>        </item>
        <item>
            <title>Pien Tze Huang inhibits tumor cell proliferation and promotes apoptosis             via suppressing the STAT3 pathway in a colorectal cancer mouse model.</title>
            <link>http://www.medworm.com/index.php?rid=5579182&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22218594%26dopt%3DAbstract</link>
            <description>Pien Tze Huang inhibits tumor cell proliferation and promotes apoptosis       via suppressing the STAT3 pathway in a colorectal cancer mouse model.
    Int J Oncol. 2012 Jan 3;
    Authors: Zhuang Q, Hong F, Shen A, Zheng L, Zeng J, Lin W, Chen Y, Sferra TJ, Hong Z, Peng J
    Abstract
    Signal transducer and activator of transcription 3 (STAT3) plays a critical       role in cell survival and proliferation. Constitutive activation of STAT3 is strongly       correlated with pathogenesis of various types of malignant tumors including colorectal       cancer (CRC), and therefore is a major focus in the development of anti-cancer       agents. Pien Tze Huang (PZH), a well-known traditional Chinese formula prescribed       already in the Ming Dynasty, has been demonstrated to be clinically e...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579182</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579182</guid>        </item>
        <item>
            <title>DNA hypomethylation at the ZNF206-exon 5 CpG island associated with             neuronal differentiation in mice and development of neuroblastoma in humans.</title>
            <link>http://www.medworm.com/index.php?rid=5382254&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22011711%26dopt%3DAbstract</link>
            <description>In this study       methylation level of the CpG sites at Zfp206-exon 5 CpGi in mouse brain samples       at three different developmental stages (15-day-old embryo; E15, new born; NB,       12-week adult; AD) were quantitatively analyzed and it was identified that Zfp206-exon       5 CpGi was the DS-DMRs in mouse brain. In AD brains, Zfp206-exon 5 CpGi was significantly       hypomethylated and Zfp206 expression was repressed, compared with E15 and NB brains.       Hence, methylation level of human 5'-end of CpGi at ZNF206-exon 5, which is homologous       CpGi to mice, was analyzed in neuroblastomas. Although all four adrenal samples       showed complete methylation at the homologous region, we found the hypomethylation       in 7 out of 26 neuroblastomas and a significant association b...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382254</comments>
            <pubDate>Mon, 07 Nov 2011 15:25:18 +0100</pubDate>
            <guid isPermaLink="false">5382254</guid>        </item>
        <item>
            <title>The potent peptide antagonist to angiogenesis, C16Y, and cisplatin act synergistically in the down-regulation of the Bcl-2/Bax ratio and the induction of apoptosis in human ovarian cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5264074&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935568%26dopt%3DAbstract</link>
            <description>We examined the effect of cisplatin alone and in combination with C16Y, a newly-identified anti-angiogenic peptide from the NH2-terminal domains of the γ-chain of laminin-1, on the modulation of Bcl-2/Bax expression and induction of apoptosis in ovarian cancer cells (OVACAR3). C16Y did not elicit cell death of human umbilical vein endothelial cells (HUVECs). Cisplatin exerted a lethal effect with an EC50 of 10 µM in OVACAR3s. In the presence of 25 or 50 µg/ml of C16Y (a range which has no effect against HUVECs), the EC50 for cisplatin in OVACAR3s decreased to 3.5 and 2.0 µM, respectively. Using fluorescence-activated cell sorting (FACS) analysis of DNA stained OVACAR3s and terminal deoxynucleotide tranferase-mediated dUTP nick end-labeling (TUNEL), we found that even at concentratio...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5264074</comments>
            <pubDate>Thu, 29 Sep 2011 20:57:36 +0100</pubDate>
            <guid isPermaLink="false">5264074</guid>        </item>
        <item>
            <title>Chronic administration of green tea extract to TRAMP mice induces the collapse of Golgi apparatus in prostate secretory cells and results in alterations of protein post-translational processing.</title>
            <link>http://www.medworm.com/index.php?rid=5264073&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935569%26dopt%3DAbstract</link>
            <description>Authors: Davalli P, Rizzi F, Caldara GF, Davoli S, Corti A, Silva A, Astancolle S, Vitale M, Bettuzzi S, Arcari M, Azzali G
    Abstract
    Considering its long latency, prostate cancer (PCa) represents an ideal target for chemoprevention strategies. Green tea extract (GTE) has been proved to be one of the most promising natural substances capable of inhibiting PCa progression in animal models (transgenic adenocarcinoma of mouse prostate), as well as in humans. However, the cellular targets of the GTE action are mostly unknown. The main objective of this work was to investigate whether the endoplasmic reticulum (ER) and the Golgi apparatus (GA), known to be actively involved in sensing stress stimuli and initiating and propagating cell death signalling, may represent the subcellular targe...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5264073</comments>
            <pubDate>Thu, 29 Sep 2011 20:56:47 +0100</pubDate>
            <guid isPermaLink="false">5264073</guid>        </item>
        <item>
            <title>Deciphering the role of paclitaxel in the SKGT4 human esophageal adenocarcinoma cell line.</title>
            <link>http://www.medworm.com/index.php?rid=5264072&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21935570%26dopt%3DAbstract</link>
            <description>In conclusion, our results suggest that paclitaxel leads to mitotic cell cycle arrest following G2/M arrest and induces apoptosis via a caspase-3 pathway in SKGT4 cells.
    PMID: 21935570 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5264072</comments>
            <pubDate>Thu, 29 Sep 2011 20:55:53 +0100</pubDate>
            <guid isPermaLink="false">5264072</guid>        </item>
        <item>
            <title>Effects of fish oil and Tamoxifen on preneoplastic lesion development and biomarkers of oxidative stress in the early stages of N-methyl-N-nitrosourea-induced rat mammary carcinogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5220275&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21892590%26dopt%3DAbstract</link>
            <description>Authors: Manni A, Richie JP, Xu H, Washington S, Aliaga C, Cooper TK, Bruggeman R, Das A, Prokopczyk B, Calcagnotto A, Trushin N, Dickinson R, Liao J, Verderame MF, El-Bayoumy K
    Abstract
    Epidemiologic studies on the protective role of omega-3 fatty acids (n:3) on breast cancer prevention remain inconclusive but studies in preclinical models provide more positive outcome. However, the mechanisms accounting for the protective effect of n:3 are not defined. In the present study, conducted in the N-methyl-N-nitrosourea-induced rat mammary carcinogenesis model, we examined the effects of n:3 individually and in combination with the anti-estrogen Tamoxifen (Tam) on a comprehensive panel of systemic and preneoplastic mammary gland restricted biomarkers which may be critical in the progres...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220275</comments>
            <pubDate>Thu, 15 Sep 2011 13:16:12 +0100</pubDate>
            <guid isPermaLink="false">5220275</guid>        </item>
        <item>
            <title>Gene expression profiles predicting the response to IFN-β and a combination of temozolomide and IFN-β in malignant gliomas.</title>
            <link>http://www.medworm.com/index.php?rid=5107015&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805051%26dopt%3DAbstract</link>
            <description>We present a list of the most highly upregulated and downregulated genes which may be involved in conferring a response to IFN-β and synergistic effect between IFN-β and TMZ in malignant gliomas. Although the present study has several limitations, our reported candidate genes could represent not only potential molecular markers but also chemotherapy targets for improving the treatment outcome by devising strategies that are able to circumvent primary drug resistance in malignant gliomas.
    PMID: 21805051 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107015</comments>
            <pubDate>Tue, 09 Aug 2011 12:30:25 +0100</pubDate>
            <guid isPermaLink="false">5107015</guid>        </item>
        <item>
            <title>Human lung fibroblasts prematurely senescent after exposure to ionizing radiation enhance the growth of malignant lung epithelial cells in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5107014&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21814715%26dopt%3DAbstract</link>
            <description>Authors: Papadopoulou A, Kletsas D
    Cellular senescence, being the result of serial subculturing or of exogenous stresses, is considered to be a potent anticancer mechanism. However, it has been proposed that senescent cells may enhance the growth of adjacent malignant epithelial cells. On the other hand, exposure of tumors to repeated low doses of γ-irradiation is a common treatment regime. Nevertheless, γ-irradiation also affects the neighboring stromal cells and the interaction of the latter with cancer cells. Accordingly, in this study, we have exposed confluent cultures of human lung fibroblasts to repeated subcytotoxic doses of 4 Gy of γ-irradiation. We found that a single dose immediately activates a DNA damage response, leading to an intense, but reversible, cell cycle arrest...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107014</comments>
            <pubDate>Tue, 09 Aug 2011 12:30:21 +0100</pubDate>
            <guid isPermaLink="false">5107014</guid>        </item>
        <item>
            <title>Tobacco-specific carcinogen nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone induces AKT activation in head and neck epithelia.</title>
            <link>http://www.medworm.com/index.php?rid=5107013&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822536%26dopt%3DAbstract</link>
            <description>Authors: Weber SM, Bornstein S, Li Y, Malkoski SP, Wang D, Rustgi AK, Kulesz-Martin MF, Wang XJ, Lu SL
    Exposure to tobacco carcinogens is causally associated with head and neck squamous cell carcinoma (HNSCC), but the underlying molecular mechanisms remain unclear. Here, we reported that AKT is activated at a higher frequency in both HNSCC tumors and the adjacent mucosa from HNSCC patients who are smokers than those from HNSCC patients who are non-smokers. Adding physiologically relevant concentrations of 4-(methylnitrosamino)-1-(3-pyridyl)-1-1butanone (NNK), a major tobacco carcinogen, to normal head and neck epithelial cells and HNSCC cell lines, rapidly and constitutively activated AKT through phosphorylation in a dose- and time-dependent manner. AKT phosphorylation was associated w...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107013</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107013</guid>        </item>
        <item>
            <title>Evidence for cardiac atrophic remodeling in cancer-induced cachexia in mice.</title>
            <link>http://www.medworm.com/index.php?rid=5107012&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21822537%26dopt%3DAbstract</link>
            <description>Authors: Tian M, Asp ML, Nishijima Y, Belury MA
    Cachexia is a common complication in cancer patients, which dramatically reduces quality of life and survival. In contrast to the well-studied feature of skeletal muscle loss, alterations in cardiac muscle are unclear. Recently, we reported that heart contractile function was significantly impaired in mice with colon-26 (C26) tumors, a widely used rodent model of cancer cachexia. In the present study, we investigated the potential underlying mechanisms for decreased heart function, specifically related to cardiac remodeling and atrophy. In cachectic mice bearing C26 tumors compared to mice without tumors, there was a gene expression pattern for cardiac remodeling, including increased BNP and c-fos, decreased PPARα and its responsive gene...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107012</comments>
            <pubDate>Thu, 04 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107012</guid>        </item>
        <item>
            <title>Antitumor and apoptosis-promoting properties of emodin, an anthraquinone derivative from Rheum officinale Baill, against pancreatic cancer in mice via inhibition of Akt activation.</title>
            <link>http://www.medworm.com/index.php?rid=5107017&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805032%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether emodin could enhance the anticancer effect of gemcitabine on pancreatic cancer in vivo. We demonstrated that treatment of gemcitabine combined with emodin efficiently suppressed tumor growth in mice inoculated with pancreatic tumor cells. This treatment paradigm promoted apoptotic cell death and mitochondrial fragmentation. Furthermore, it reduced phosphorylated-Akt (p-Akt) level, NF-κB activation and Bcl-2/Bax ratio, increased caspase-9 and -3 activation, Cytochrome C (CytC) release occurred in combination therapy. Collectively, emodin enhanced the activity of gemcitabine in tumor growth suppression via inhibition of Akt and NF-κB activation, thus promoting the mitochondrial-dependent apoptotic pathway. Therefore, our findings may provide new insig...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107017</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107017</guid>        </item>
        <item>
            <title>Inhibition of induced autophagy increases apoptosis of Nara-H cells.</title>
            <link>http://www.medworm.com/index.php?rid=5107016&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805033%26dopt%3DAbstract</link>
            <description>Authors: Nakamura O, Hitora T, Akisue T, Kawamoto T, Yamagami Y, Yamamoto T
    Inhibition of the mTOR signaling pathway promotes initiation of autophagy. However, recent studies indicate that autophagy is a self-defense mechanism of cancer cells that are subjected to anti-tumor agents and that blocking autophagy can trigger apoptosis. Here, we examined the effects of an mTOR inhibitor, temsirolimus, on a malignant fibrous histiocytoma (MFH) cell line, Nara-H cells, and the effect of suppressing autophagy on the induction of apoptosis in these MFH cells. In Nara-H cells, we examined the effects of temsirolimus treatment on cell proliferation using the CellTiter 96® AQueous One Solution Cell Proliferation Assay and on phosphorylation of mTOR pathway components and autophagy using Western b...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107016</comments>
            <pubDate>Thu, 28 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107016</guid>        </item>
        <item>
            <title>A murine model of hepatitis B-associated hepatocellular carcinoma generated by adeno-associated virus-mediated gene delivery.</title>
            <link>http://www.medworm.com/index.php?rid=5107019&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805030%26dopt%3DAbstract</link>
            <description>Authors: Huang YH, Fang CC, Tsuneyama K, Chou HY, Pan WY, Shih YM, Wu PY, Chen Y, Leung PS, Gershwin ME, Tao MH
    A relevant animal model is critical for investigating the pathogenic mechanisms underlying hepatitis B virus (HBV)-induced hepatocellular carcinoma (HCC). Mice are not naturally infected by HBV, presumably due to the lack of HBV receptors on mouse hepatocytes. To bypass this entry step of HBV infection, we report generation of a novel HBV model in immunocompetent mice by hepatic delivery of the HBV genome using trans-splicing adeno-associated viral vectors (AAV/HBV). We confirmed production of HBV virions and proteins in the liver and circulation in all AAV/HBV-transduced mice in all four immunocompetent mouse strains tested. These mice produced antigen and antibody profiles ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107019</comments>
            <pubDate>Wed, 27 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107019</guid>        </item>
        <item>
            <title>Comparison of different classes of CpG-ODN in augmenting the generation of human epitope peptide-specific CTLs.</title>
            <link>http://www.medworm.com/index.php?rid=5107018&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805031%26dopt%3DAbstract</link>
            <description>Authors: Katsuda M, Iwahashi M, Matsuda K, Miyazawa M, Nakamori M, Nakamura M, Ojima T, Iida T, Hayata K, Yamaue H
    Three distinct classes of CpG-oligonucleotides (ODN) (CpG-A, CpG-B and CpG-C) have been identified on the basis of differences in their structures and immune effects. To date, only CpG-B is applied for clinical treatments; however, it is still unknown which of the different CpG-ODN classes is most useful as an adjuvant for human cancer vaccine therapy. In the present study, we examined the activity of these 3 types of CpG-ODN in enhancing the induction of human peptide-specific CTLs. Our data showed that the specific cytotoxicity was augmented in the presence of CpG-A, -B and -C but not in the presence of control ODN, and the augmenting effect was most potent with CpG-A. F...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107018</comments>
            <pubDate>Wed, 27 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107018</guid>        </item>
        <item>
            <title>Involvement of EGFR in the promotion of malignant properties in multidrug resistant breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5107021&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805028%26dopt%3DAbstract</link>
            <description>In conclusion, EGFR is an important factor enhancing the malignancy of MDR breast cancer cells, partially, inducing MDR. Anti-EGFR therapy may improve outcome in chemorefractory breast cancer patients.
    PMID: 21805028 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107021</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107021</guid>        </item>
        <item>
            <title>Upregulation of NKG2D ligands and enhanced natural killer cell cytotoxicity by hydralazine and valproate.</title>
            <link>http://www.medworm.com/index.php?rid=5107020&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21805029%26dopt%3DAbstract</link>
            <description>In conclusion, our results demonstrate the ability of hydralazine and valproate to increase the NK activity against epithelial cancer cell lines and suggest that these drugs could reduce the levels of soluble MICA and MICB helping in avoiding tumor-induced suppression of NK cytotoxicity against the tumor.
    PMID: 21805029 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107020</comments>
            <pubDate>Mon, 25 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107020</guid>        </item>
        <item>
            <title>A novel function of EpCAM in oral squamous cell carcinoma cells under anchorage-independent conditions.</title>
            <link>http://www.medworm.com/index.php?rid=5107027&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785818%26dopt%3DAbstract</link>
            <description>Authors: Inoue H, Ohnishi Y, Nakajima M, Kakudo K, Nozaki M
    Epithelial cell adhesion molecule (EpCAM), involved in Ca2+-independent homotypic cell-cell adhesion in epithelial tissues, is overexpressed in several cancer types. Although studies investigating the function of EpCAM in cancers have shown that it plays a role in cell proliferation, invasion and metastasis, the overall function of EpCAM in cancer cells has remained elusive. Here, we report a novel function of EpCAM in multicellular aggregates (MCAs). EpCAM inhibition using RNA interference (RNAi) did not affect cell morphology, proliferation or expression of certain genes, including cyclin D1 in monolayer cultures of the human oral squamous cell carcinoma cell lines HSC-3 or HSC-4. However, in HSC-4 cells cultured as MCAs, su...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107027</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107027</guid>        </item>
        <item>
            <title>Tumor-derived vascular endothelial growth factor (VEGF)-A facilitates tumor metastasis through the VEGF-VEGFR1 signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5107026&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785819%26dopt%3DAbstract</link>
            <description>In this study, we show that in cancer patients high expression of VEGF is correlated with metastasis, and anti-VEGF treatment (bevacizumab) has clinical effects on tumor metastasis. Two human lung carcinoma cell lines (A549 and SPCA1 cells) with distinct VEGF expression were injected intravenously through the lateral tail vein of SCID mice and a murine model was developed. We investigated the association between the expression of VEGF and tumor metastasis by microvessel density, immunohistochemistry and whole mount staining. At sacrifice, in the high VEGF expression A549 cell line group, the induced tumor was distinctively larger in size and multiple metastatic lesions were found in lung tissues. Two specific neutralizing anti-mouse VEGFR1 and VEGFR2 antibodies were administered to the tum...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107026</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107026</guid>        </item>
        <item>
            <title>Model examinatio-n of chemoprevention with retinoids in squamous cell carcinomas of the head and neck region and suitable biomarkers for chemoprevention.</title>
            <link>http://www.medworm.com/index.php?rid=5107025&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785820%26dopt%3DAbstract</link>
            <description>In this study, cell culture models are used to demonstrate immunocytochemical expression of RA receptors (RAR, RXR), Ki-67 and p53 before and after all-trans retinoic acid (ATRA) treatment. Telomerase activity in PCR is used to assess the effectiveness of ATRA. Along with an RA-sensitive HNSCC cell line UM-SCC-35 we employed cell lines UM-SCC-14C and HaCaT. Our immunocytochemical examination produced no proof of a statistically significant change in expression of RARα, RARβ or RXRγ receptors after ATRA treatment, either in the cells of the sensitive UM-SCC-35 line or in HaCaT cells. The RARβ and RXRγ receptors showed increased expression after brief cell treatment of UM-SCC-14C. The reduced telomerase activity after prolonged treatment of the UM-SCC-35-cells with ATRA (as well as the ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107025</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107025</guid>        </item>
        <item>
            <title>Androgen deprivation therapy affects BCL-2 expression in human prostate cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5107024&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785821%26dopt%3DAbstract</link>
            <description>Authors: Fuzio P, Ditonno P, Lucarelli G, Battaglia M, Bettocchi C, Senia T, Perlino E
    BCL-2 is an integral protein of the external mitochondrial membrane that inhibits cell apoptotic death. We investigated the effect of androgen deprivation therapy (ADT) on BCL-2 expression in prostate cancer tissues. We studied BCL-2 expression in vivo in prostate cancer tissues obtained from patients who underwent radical prostatectomy after neoadjuvant ADT, by Northern and Western blot analysis, and immunohistochemistry. Moreover, gene transcriptional activity was also measured by nuclear run-on experiments. We demonstrated an increase of BCL-2 mRNA expression in patients who underwent neoadjuvant ADT for 1 month in comparison to patients who had not received any therapy. Moreover, we demonstrated ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107024</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107024</guid>        </item>
        <item>
            <title>Anti-tumor activity of the proteasome inhibitor bortezomib in gastric cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5107023&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785822%26dopt%3DAbstract</link>
            <description>We examined the anti-tumor effects of bortezomib on gastric cancer cells in vitro and in subcutaneously transplanted nude mice. We demonstrated that among seven types of gastric cancer cells examined, treatment with bortezomib induced both apoptotic and anti-proliferative effects, resulting in a reduction in cell survival rates. The induction of apoptosis was observed to be dependent on the inhibition of nuclear factor κB (NF-κB) activation and the subsequent production of reactive oxygen species (ROS) and c-Jun N-terminal kinase (JNK) activation. Interestingly, we observed that those cells with high levels of NF-κB activity were resistant to bortezomib treatment. Additionally, we demonstrated that the activation of the extracellular signal-regulated kinase (ERK1/2) was inhibited follo...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107023</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107023</guid>        </item>
        <item>
            <title>Three-dimensional culture promotes reconstitution of the tumor-specific hypoxic microenvironment under TGFβ stimulation.</title>
            <link>http://www.medworm.com/index.php?rid=5107022&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785823%26dopt%3DAbstract</link>
            <description>Authors: Marushima H, Shibata SI, Asakura T, Matsuura T, Maehashi H, Ishii Y, Eda H, Aoki K, Iida Y, Morikawa T, Ohkawa K
    In vitro tumor growth in a three-dimensional (3D) architecture has been demonstrated to play an important role in biology not only for developmental organogenesis and carcinogenesis, but also for analyses on reconstitution and maintenance in a variety of biological environments surrounding the cells. In addition to providing architectural similarity to living organisms, 3D culture with a radial flow bioreactor (RFB) can also closely mimic the living hypoxic microenvironment under which specific organogenesis or carcinogenesis occurs. The findings of the present study under the RFB culture conditions show that cancer cells underwent a shift from aerobic to hypoxic en...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5107022</comments>
            <pubDate>Thu, 21 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5107022</guid>        </item>
        <item>
            <title>miRNAs can predict prostate cancer biochemical relapse and are involved in tumor progression.</title>
            <link>http://www.medworm.com/index.php?rid=5062763&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769427%26dopt%3DAbstract</link>
            <description>Authors: Fendler A, Jung M, Stephan C, Honey RJ, Stewart RJ, Pace KT, Erbersdobler A, Samaan S, Jung K, Yousef GM
    Prostate cancer is the leading cancer diagnosed and the second most common cause of cancer related death in the western world. For prognostic monitoring after prostatectomy, recurrent increase of prostate-specific antigen (PSA), the so-called PSA or biochemical relapse remains the leading biomarker. There is currently no biomarker that can accurately predict the risk of relapse at the time of surgery. We analyzed formalin-fixed and paraffin-embedded tissue samples from 52 primary prostate cancers and normal adjacent tissues obtained after radical prostatectomy. Patients were grouped into two categories: i) patients with early biochemical relapse (&amp;lt;1 year after radical pr...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062763</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062763</guid>        </item>
        <item>
            <title>Redistribution of DR4 and DR5 in lipid rafts accounts for the sensitivity to TRAIL in NSCLC cells.</title>
            <link>http://www.medworm.com/index.php?rid=5062762&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769428%26dopt%3DAbstract</link>
            <description>In this study, compared to TRAIL-sensitive H460 cell line, TRAIL-resistant A549 cell line showed a similar expression level of DR5 and a higer expression level of DR4. It indicates that there is no positive correlation between the expression levels of death receptors and sensitivity to TRAIL. However, tests on A549 cells with DR4 siRNA transfection revealed that DR4-competitive binding to TRAIL could not affect the capacity of TRAIL in inducing apoptosis. Instead, further studies found that the aggregation of DR4 and DR5 in lipid rafts only occured in H460 cells with TRAIL pretreatment. It suggested that the TRAIL-induced redistribution of DR4 and DR5 in lipid rafts contributed to the sensitivity to TRAIL in TRAIL-sensitive NSCLC H460 cell line, which was also confirmed by intervention tes...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062762</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062762</guid>        </item>
        <item>
            <title>Herpesvirus saimiri-mediated delivery of the adenomatous polyposis coli tumour suppressor gene reduces proliferation of colorectal cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5062761&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769429%26dopt%3DAbstract</link>
            <description>Authors: Macnab SA, Turrell SJ, Carr IM, Markham AF, Coletta PL, Whitehouse A
    Colorectal cancer (CRC) is a major cause of cancer-related mortality. A contributing factor to the progression of this disease is sporadic or hereditary mutation of the adenomatous polyposis coli (APC) gene, a negative regulator of the Wnt signalling pathway. Inherited mutations in APC cause the disorder familial adenomatous polyposis (FAP), which leads to CRC development in early adulthood. However, the gene is also disrupted in some 60% of sporadic cancers. Restoration of functional APC may slow the growth of CRC by negatively regulating proliferation-associated genes such as c-myc. Therefore, we have cloned the cDNA of the APC tumour suppressor gene into a replication competent Herpesvirus saimiri (HVS)-ba...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062761</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062761</guid>        </item>
        <item>
            <title>Narrow band imaging hysteroscopy: A comparative study using randomized video images.</title>
            <link>http://www.medworm.com/index.php?rid=5062760&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769430%26dopt%3DAbstract</link>
            <description>Authors: Kisu I, Banno K, Kobayashi Y, Ono A, Masuda K, Ueki A, Nomura H, Hirasawa A, Abe T, Kouyama K, Susumu N, Aoki D
    Narrow band imaging (NBI) has been used in the gastrointestinal endoscopy field as a novel endoscopic imaging technique and has contributed to improved qualitative diagnosis and detection of lesions. However, there are only a few studies of use of NBI in the gynecology field. We applied NBI in flexible hysteroscopy at our outpatient clinic and evaluated the utility of NBI hysteroscopy for diagnosis of malignant endometrial lesions by comparison of the sensitivity and specificity between white light alone and white light+NBI using hysteroscopic video images. The subjects were 65 patients with a suspected endometrial lesion in the uterine cavity. These patients underwe...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062760</comments>
            <pubDate>Sun, 17 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062760</guid>        </item>
        <item>
            <title>NF-κB induces abnormal centrosome amplification by upregulation of CDK2 in laryngeal squamous cell cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5062766&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769424%26dopt%3DAbstract</link>
            <description>Authors: Liu JL, Ma HP, Lu XL, Sun SH, Guo X, Li FC
    Centrosome amplification can drive chromosomal instability (CIN) which is a major source of tumor initiation. The present study aimed to investigate the impact of nuclear factor kappa B (NF-κB) on centrosome amplification of Hep-2 cells. Immunofluorescence was performed to display centrosomes. BAY11-7082 was used as an inhibitor of NF-κB to assess the inhibition of centrosome amplification, and cyclin-dependent kinase 2 (CDK2), ensuring cell cycle cycle coordination with centrosome cycle was detected by Western blotting. Furthermore, a 1556-bp fragment of the CDK2 promoter was analyzed using the TRANSFAC-TESS software. Luciferase assay, including a series of truncated CDK2 promoters and site mutations, was carried out to determine N...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062766</comments>
            <pubDate>Thu, 14 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062766</guid>        </item>
        <item>
            <title>Genetically engineered stem cells expressing cytosine deaminase and interferon-β migrate to human lung cancer cells and have potentially therapeutic anti-tumor effects.</title>
            <link>http://www.medworm.com/index.php?rid=5062765&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769425%26dopt%3DAbstract</link>
            <description>Authors: Yi BR, O SN, Kang NH, Hwang KA, Kim SU, Jeung EB, Kim YB, Heo GJ, Choi KC
    Recent studies have shown that genetically engineered stem cells (GESTECs) produce suicide enzymes that convert non-toxic pro-drugs to toxic metabolites which selectively migrate toward tumor sites and reduce tumor growth. In the present study, we evaluated whether these GESTECs are capable of migrating to lung cancer cells and examined the potential therapeutic efficacy of gene-directed enzyme pro-drug therapy against lung cancer cells in vitro. A modified transwell migration assay was performed to determine the migratory capacity of GESTECs to lung cancer cells. GESTECs [i.e., HB1.F3.CD or HB1.F3.CD.interferon-β (IFN-β)] engineered to express a suicide gene, cytosine deaminase (CD), selectively migra...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062765</comments>
            <pubDate>Thu, 14 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062765</guid>        </item>
        <item>
            <title>Cathepsin L is highly expressed in gastrointestinal stromal tumors.</title>
            <link>http://www.medworm.com/index.php?rid=5062764&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769426%26dopt%3DAbstract</link>
            <description>Authors: Miyamoto K, Iwadate M, Yanagisawa Y, Ito E, Imai JI, Yamamoto M, Sawada N, Saito M, Suzuki S, Nakamura I, Ohki S, Saze Z, Kogure M, Gotoh M, Omicronbara K, Ohira H, Tasaki K, Abe M, Goshima N, Watanabe S, Waguri S, Takenoshita S
    Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract that are diagnosed by c-kit staining in most cases. A lysosomal cysteine proteinase termed cathepsin L has been commonly associated with malignancy in several cancer types, but this finding has not been reported for GISTs. We analyzed the cathepsin L mRNA and protein expression in GISTs. Real-time reverse transcription polymerase chain reaction (RT-PCR) analysis revealed that cathepsin L levels were higher in GISTs than those in gastric or color...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062764</comments>
            <pubDate>Thu, 14 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062764</guid>        </item>
        <item>
            <title>Epiregulin as a marker for the initial steps of ovarian cancer development.</title>
            <link>http://www.medworm.com/index.php?rid=5062768&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769422%26dopt%3DAbstract</link>
            <description>Authors: Amsterdam A, Shezen E, Raanan C, Slilat Y, Ben-Arie A, Prus D, Schreiber L
    Epiregulin (Ep) was found to be produced in non-cancer ovarian cells in response to gonadotropin stimulation as well in ovarian cancer cells in an autonomous manner. However, there were no systematic follow-up studies of Ep expression in the development of different stages of ovarian cancer. Using specific antibodies to Ep and the indirect immunocytochemistry methods, we found that in normal ovary the staining for Ep was mainly confined to the epithelial cells, while the stromal cells were only occasionally and moderately stained. In contrast in benign serous and mucinous tumors most of the tumor cells showed a clear staining in the cytoplasm. In borderline serous and mucinous tumors the staining was mu...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062768</comments>
            <pubDate>Wed, 13 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062768</guid>        </item>
        <item>
            <title>Induction of specific human cytotoxic T cells using dendritic cells transduced with an adenovector encoding rat epidermal growth factor receptor 2.</title>
            <link>http://www.medworm.com/index.php?rid=5062767&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769423%26dopt%3DAbstract</link>
            <description>This study demonstrates the ability to generate antigen-specific cytotoxic T cells (CTLs) against HER2 using a xenoantigenic immune stimulation strategy. Dendritic cells (DCs) were transduced with an adenovirus vector incorporating full-length cDNA for rat (xenoantigen) epidermal growth factor receptor 2 (Adv-HER2). Stimulation of autologous T cells with Adv-HER2 infected DCs led to enhanced HER2-specific reactivity as assessed by quantitative real-time polymerase chain reaction (qRT-PCR) for T cell IFN-γ mRNA. In ELISPOT and intracellular cytokine staining (ICS) assays, CD8+ CTLs induced by Adv-HER2 transduced DCs released IFN-γ following stimulation with irradiated autologous DCs infected with Adv-HER2 or loaded with a human prostate cancer cell line (LNCaP) lysate. DCs pulsed with HER...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062767</comments>
            <pubDate>Wed, 13 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062767</guid>        </item>
        <item>
            <title>Gene expression of vasoactive intestinal peptide receptors in human lung cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5062769&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21769421%26dopt%3DAbstract</link>
            <description>Authors: Szilasi M, Buglyo A, Treszl A, Kiss L, Schally AV, Halmos G
    Despite significant improvement in the diagnosis and treatment of various human carcinomas, the 5-year survival rate for lung cancer remains below 20%. Vasoactive intestinal peptide (VIP) is an important neuropeptide in the control of lung physiology, and exerts its functions mainly through two receptor subtypes, VPAC1 and VPAC2. Receptors for VPAC1 and VPAC2 are present in human lung cancer cells, but very limited information exists about the mRNA expression of these VIP receptor subtypes in lung cancer specimens. The aim of the present study was to investigate by RT-PCR the mRNA expression of the VPAC1 and VPAC2 receptors in surgical specimens of 43 human lung cancer specimens and 7 normal lung samples. mRNA express...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062769</comments>
            <pubDate>Tue, 12 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062769</guid>        </item>
        <item>
            <title>MYCN amplicon junctions as tumor-specific targets for minimal residual disease detection in neuroblastoma.</title>
            <link>http://www.medworm.com/index.php?rid=5062771&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750863%26dopt%3DAbstract</link>
            <description>This study provides new information on the mechanisms of oncogene amplification and envisages means of rapidly obtaining highly sensitive PCR-based tools for tumor/patient-specific monitoring of treatment response and the early detection of relapse in patients with neuroblastoma.
    PMID: 21750863 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062771</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062771</guid>        </item>
        <item>
            <title>The BH3-only protein Noxa is stimulated during apoptosis of chronic lymphocytic leukemia cells triggered by M2YN, a new plant-derived extract.</title>
            <link>http://www.medworm.com/index.php?rid=5062770&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750864%26dopt%3DAbstract</link>
            <description>Authors: Zaher M, Mirshahi M, Nuraliev Y, Sharifova M, Bombarda I, Marie JP, Billard C
    Deficiency of apoptosis is a hallmark of chronic lymphocytic leukemia (CLL) cells. M2Yn is a natural extract from plants of central Asia, identified for its antiangiogenic properties and its ability to block the migration of malignant cells. Here, we report that in vitro treatment of cells derived from CLL patients with M2Yn results in internucleosomal DNA fragmentation, phosphatidylserine externalization, mitochondrial membrane depolarization, caspase-3 activation and cleavage of the caspase substrate PARP-1. The extents of these effects depend on the patients and are mostly comparable to those of flavopiridol or hyperforin, two known plant-derived apoptosis inducers of CLL cells. M2Yn does not modu...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062770</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062770</guid>        </item>
        <item>
            <title>Protein profiling of angiogenesis-related growth factors in laryngeal carcinoma: Pattern of protein expression in relation to tumour progression.</title>
            <link>http://www.medworm.com/index.php?rid=5062774&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743965%26dopt%3DAbstract</link>
            <description>In conclusion, this study has identified a number of factors involved in angiogenesis that are likely to contribute to the growth and metastasis of laryngeal tumours. Furthermore, a number of factors were also substantially altered in metastatic deposits compared with the primary tumour mass or adjacent normal tissue. This study requires confirmatory analysis of the selected key factors in a larger cohort of patients.
    PMID: 21743965 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062774</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062774</guid>        </item>
        <item>
            <title>The effect of p-4E-BP1 and p-eIF4E on cell proliferation in a breast cancer model.</title>
            <link>http://www.medworm.com/index.php?rid=5062773&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750861%26dopt%3DAbstract</link>
            <description>Authors: Pons B, Peg V, Vázquez-Sánchez MA, López-Vicente L, Argelaguet E, Coch L, Martínez A, Hernández-Losa J, Armengol G, Ramon Y Cajal S
    Cell signaling pathways and protein translation are crucial for understanding malignant transformation. 4E-BP1 and the eIF4F complex regulate cap-dependent translation. We investigated how 4E-BP1 and eIF4E phosphorylation status affects in vitro and in vivo cell proliferation in a breast cancer model. Cells from 2 breast carcinoma lines (MDA-MB 231 and MDA-MB 468) and human fibroblasts (IMR90 cells) were infected in vitro with a retrovirus carrying a wild-type 4E-BP1 or a mutant 4E-BP1 unable to hyperphosphorylate. Overexpression of the mutant 4E-BP1 induced a significant decrease in cell proliferation in IMR90 and MDA-MB 468 cells, but not i...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062773</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062773</guid>        </item>
        <item>
            <title>Relocalization of cell adhesion molecules during neoplastic transformation of human fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=5062772&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750862%26dopt%3DAbstract</link>
            <description>Authors: Belgiovine C, Chiodi I, Mondello C
    Studying neoplastic transformation of telomerase immortalized human fibroblasts (cen3tel), we found that the transition from normal to tumorigenic cells was associated with the loss of growth contact inhibition, the acquisition of an epithelial-like morphology and a change in actin organization, from stress fibers to cortical bundles. We show here that these variations were paralleled by an increase in N-cadherin expression and relocalization of different adhesion molecules, such as N-cadherin, α-catenin, p-120 and β-catenin. These proteins presented a clear membrane localization in tumorigenic cells compared to a more diffuse, cytoplasmic distribution in primary fibroblasts and non-tumorigenic immortalized cells, suggesting that tumorigeni...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062772</comments>
            <pubDate>Thu, 07 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062772</guid>        </item>
        <item>
            <title>Enhanced antitumor efficacy by the combination of emodin and gemcitabine against human pancreatic cancer cells via downregulation of the expression of XIAP in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5062776&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743963%26dopt%3DAbstract</link>
            <description>This study suggests that emodin enhances the antitumor effect of gemcitabine in SW1990 pancreatic cancer in vitro and in vivo, which may be via the downregulation of NF-κB expression, thus inhibiting the expression of XIAP.
    PMID: 21743963 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062776</comments>
            <pubDate>Tue, 05 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062776</guid>        </item>
        <item>
            <title>The dietary flavonol fisetin enhances the apoptosis-inducing potential of TRAIL in prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5062775&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743964%26dopt%3DAbstract</link>
            <description>This study was designed to investigate the effect of fisetin on the TRAIL-induced apoptosis potential in prostate cancer cells. Prostate cancer cell lines represent an ideal model for research in chemoprevention. Cytotoxicity was measured by MTT and LDH assays. Apoptosis was detected using Αnnexin V-FITC by flow cytometry and fluorescence microscopy. Mito-chondrial membrane potential (ΔΨm) was evaluated using DePsipher staining by fluorescence microscopy. Death receptor (TRAIL-R1 and TRAIL-R2) expression was analysed by flow cytometry. Inhibition of NF-κB (p65) activation was confirmed with an ELISA-based TransAM NF-κB kit. Caspase-8 and caspase-3 activities were determined by colorimetric protease assays. Our study demonstrates that fisetin sensitizes the TRAIL-resistant androgen-de...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062775</comments>
            <pubDate>Tue, 05 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062775</guid>        </item>
        <item>
            <title>Prognostic impact of disseminated tumor cells and microRNA-17-92 cluster deregulation in gastrointestinal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5062779&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743960%26dopt%3DAbstract</link>
            <description>Authors: Valladares-Ayerbes M, Blanco M, Haz M, Medina V, Iglesias-Díaz P, Lorenzo-Patiño MJ, Reboredo M, Santamarina I, Figueroa A, Antón-Aparicio LM, Calvo L
    The presence of tumor cells in the bone marrow (BM) could be relevant to identifying high risk of disease progression and death in gastrointestinal cancer. However, the molecular profile associated with disseminated tumor cells (DTCs) homing to the BM has yet to be defined. MicroRNAs (miRNA) play key roles in cellular processes implicated in cancer. Thus, we investigated in 38 patients with colorectal, gastric or pancreatic cancer whether the presence of BM-DTCs is associated with a specific miRNA tumor profile and analyzed their potential prognostic impact. DTCs were detected by immunocytochemistry and anti-cytokeratin antib...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062779</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062779</guid>        </item>
        <item>
            <title>Aspirin acetylates multiple cellular proteins in HCT-116 colon cancer cells: Identification of novel targets.</title>
            <link>http://www.medworm.com/index.php?rid=5062778&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743961%26dopt%3DAbstract</link>
            <description>Authors: Marimuthu S, Chivukula RS, Alfonso LF, Moridani M, Hagen FK, Bhat GJ
    Epidemiological and clinical observations provide consistent evidence that regular intake of aspirin may effectively inhibit the occurrence of epithelial tumors; however, the molecular mechanisms are not completely understood. In the present study, we determined the ability of aspirin to acetylate and post-translationally modify cellular proteins in HCT-116 human colon cancer cells to understand the potential mechanisms by which it may exerts anti-cancer effects. Using anti-acetyl lysine antibodies, here we demonstrate that aspirin causes the acetylation of multiple proteins whose molecular weight ranged from 20 to 200 kDa. The identity of these proteins was determined, using immuno-affinity purification, mas...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062778</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062778</guid>        </item>
        <item>
            <title>Fragmented hyaluronan is an autocrine chemokinetic motility factor supported by the HAS2-HYAL2/CD44 system on the plasma membrane.</title>
            <link>http://www.medworm.com/index.php?rid=5062777&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743962%26dopt%3DAbstract</link>
            <description>Authors: Saito T, Kawana H, Azuma K, Toyoda A, Fujita H, Kitagawa M, Harigaya K
    Hyaluronan (HA) is synthesized by HA synthase (HAS) 1, HAS2 and HAS3, and degraded by hyaluronidase (HYAL) 1 and HYAL2 in a CD44-dependent manner. HA and HYALs are intricately involved in tumor growth and metastasis. Random cell movement is generally described as chemokinesis, and represents an important step at the beginning of tumor cell liberation from the primary site. To investigate the roles of HAS2 and HYAL2/CD44 in cell motility, we examined HeLa-S3 cells showing spontaneous chemokinesis. HeLa-S3 cells expressed HAS2 and HAS3. siRNA-mediated knockdown of HAS2 decreased spontaneous chemokinesis of HeLa-S3 cells. Although HeLa-S3 cells secreted 50 ng/ml of high molecular weight (HMW)-HA (peak: 990 kDa...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5062777</comments>
            <pubDate>Sun, 03 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5062777</guid>        </item>
        <item>
            <title>Neoplastic transformation by TERT in FGF-2-expanded human mesenchymal stem cells.</title>
            <link>http://www.medworm.com/index.php?rid=4874225&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573488%26dopt%3DAbstract</link>
            <description>Authors: Yamaoka E, Hiyama E, Sotomaru Y, Onitake Y, Fukuba I, Sudo T, Sueda T, Hiyama K
    The low percentage of human mesenchymal stem cells (hMSCs) in bone marrow necessitates their in vitro expansion prior to clinical use in regenerative medicine. We evaluated the effect of long-term culture of hMSCs on telomere length and transformation capacity by TERT transfection. hMSCs were isolated from the bone marrow aspirates of 24 donors and cultured with fibroblast growth factor-2 (FGF-2). Six cell lines with &amp;gt;500 population doubling levels were considered immortalized. TERT was transfected into two of the six lines for a comparison of telomere length, telomerase activity, differential capacity, colony formation capacity in soft agar and tumorigenicity in immunodeficient (NOD-SCID) mice....</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874225</comments>
            <pubDate>Sat, 28 May 2011 20:15:53 +0100</pubDate>
            <guid isPermaLink="false">4874225</guid>        </item>
        <item>
            <title>Intracellular estrogen receptor-binding fragment-associated antigen 9 exerts in vivo tumor-promoting effects via its coiled-coil region.</title>
            <link>http://www.medworm.com/index.php?rid=4874224&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573489%26dopt%3DAbstract</link>
            <description>Authors: Maeyama Y, Otsu M, Kubo S, Yamano T, Iimura Y, Onodera M, Kondo S, Sakiyama Y, Ariga T
    Estrogen receptor-binding fragment-associated antigen 9 (EBAG9) is a tumor-promoting factor of largely unknown function. To assess a causative role of EBAG9 in advanced malignancies, we generated the EG7-OVA and MethA murine tumor cell lines that stably express full-length or truncated EBAG9 protein, using retroviral-mediated gene transduction. Upon subcutaneous inoculation into immunocompetent mice, both cell lines showed marked acceleration of in vivo tumor growth when full-length EBAG9 was overexpressed. Interestingly, deletion of the coiled-coil region, thereby producing truncated EBAG9 protein, abolished the tumor-acceleration effect, establishing the importance of this domain in EBAG9-...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874224</comments>
            <pubDate>Sat, 28 May 2011 20:15:49 +0100</pubDate>
            <guid isPermaLink="false">4874224</guid>        </item>
        <item>
            <title>High incidence of high-risk HPV in benign and malignant lesions of the larynx.</title>
            <link>http://www.medworm.com/index.php?rid=4874223&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573490%26dopt%3DAbstract</link>
            <description>Authors: Duray A, Descamps G, Arafa M, Decaestecker C, Remmelink M, Sirtaine N, Ernoux-Neufcoeur P, Mutijima E, Somja J, Depuydt CE, Delvenne P, Saussez S
    The aim of this study was to determine the prevalence of human papillomavirus (HPV) in patients with laryngeal benign lesions (LBLs) and laryngeal squamous cell carcinomas (LSCCs) using a sensitive E6/E7 type-specific PCR. Paraffin-embedded samples from LBL (n=39) and LSCC patients (n=67) were evaluated for the presence of HPV DNA by GP5+/GP6+ consensus PCR and E6/E7 type-specific PCR for HPV types 6, 11, 16, 18, 31, 33, 35, 39, 45, 51, 52, 53, 56, 58, 59, 66 and 68. In LSCCs, immunohistochemical staining of p16, p53 and EGFR was also assessed. The E6/E7 type-specific PCR showed that 44 out of 59 LSCC patients (i.e., 75%) had high-ri...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874223</comments>
            <pubDate>Sat, 28 May 2011 20:15:44 +0100</pubDate>
            <guid isPermaLink="false">4874223</guid>        </item>
        <item>
            <title>Wogonin triggers apoptosis in human osteosarcoma U-2 OS cells through the endoplasmic reticulum stress, mitochondrial dysfunction and caspase-3-dependent signaling pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4874222&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573491%26dopt%3DAbstract</link>
            <description>In conclusion, wogonin induced ROS production and intracellular Ca2+, and altered the levels of anti- (Bcl-2) and pro- (Bad and Bax) apoptotic proteins. Wogonin-induced apoptosis in U-2 OS cells was through the activation of caspase-3. In conclusion, these are the first findings to show wogonin-induced cytotoxic effects through induction of apoptotic cell death and ER stress in U-2 OS cells. The potent in vitro antitumor activities suggest that wogonin could be developed for the treatment of human osteosarcoma in the future.
    PMID: 21573491 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874222</comments>
            <pubDate>Sat, 28 May 2011 20:15:37 +0100</pubDate>
            <guid isPermaLink="false">4874222</guid>        </item>
        <item>
            <title>Molecular mechanisms of the antimetastatic activity of nuclear clusterin in prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4874221&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573492%26dopt%3DAbstract</link>
            <description>Authors: Moretti RM, Mai S, Montagnani Marelli M, Rizzi F, Bettuzzi S, Limonta P
    The proapoptotic activity of nuclear clusterin (nCLU) in cancer cells is now well established. We previously showed that nCLU decreases the motility of prostate cancer cells by triggering a dramatic dismantling of the actin cytoskeleton. Here, we sought to unravel the molecular mechanisms of the antimetastatic activity of nCLU. We found that nCLU: i) decreases LIMK1 expression, thus increasing the levels of the active (unphosphorylated) form of cofilin, the well known actin depolymerizing factor; ii) binds to vimentin, sequestering the protein from its adhesion sites at the cell periphery, thus interfering with its role in cell motility and adhesion; iii) affects the intracellular distribution of E-cadheri...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874221</comments>
            <pubDate>Sat, 28 May 2011 20:15:31 +0100</pubDate>
            <guid isPermaLink="false">4874221</guid>        </item>
        <item>
            <title>Recombinant NY-ESO-1 protein with ISCOMATRIX adjuvant induces broad antibody responses in humans, a RAYS-based analysis.</title>
            <link>http://www.medworm.com/index.php?rid=4874220&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573493%26dopt%3DAbstract</link>
            <description>Authors: Mischo A, Bubel N, Cebon JS, Samaras P, Petrausch U, Stenner-Liewen F, Schaefer NG, Kubuschok B, Renner C, Wadle A
    Antibody responses to tumor antigens play an important role in initiating a cellular antitumor response with respect to antigen cross-presentation and T cell cross-priming. Successful vaccination strategies rely on an optimally timed activation of the humoral and cellular immune system by using appropriate adjuvant stimulation. The LUD99-008 trial used the cancer testis antigen NY-ESO-1 formulated with ISCOMATRIX adjuvant injected into patients intramuscularly. It was shown that this vaccination strategy is a safe and highly potent activator of the humoral and cellular immune system. Using the RAYS technology, we analyzed in detail the humoral immune response in t...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874220</comments>
            <pubDate>Sat, 28 May 2011 20:15:22 +0100</pubDate>
            <guid isPermaLink="false">4874220</guid>        </item>
        <item>
            <title>Tumor vaccine composed of CpG ODN class C and irradiated tumor cells up-regulates the expression of genes characteristic of mature dendritic cells and of memory cells.</title>
            <link>http://www.medworm.com/index.php?rid=4874219&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21573508%26dopt%3DAbstract</link>
            <description>In conclusion, our results provide insight into the nature and scope of the antitumor immune response elicited by this kind of tumor vaccine in vivo. We showed that the maturation of APCs is a prerequisite for the generation of effective long-term antitumor immunity.
    PMID: 21573508 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874219</comments>
            <pubDate>Sat, 28 May 2011 20:15:10 +0100</pubDate>
            <guid isPermaLink="false">4874219</guid>        </item>
        <item>
            <title>Phosphorylation of β-catenin results in lack of β-catenin signaling in melanoma.</title>
            <link>http://www.medworm.com/index.php?rid=4874218&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21584489%26dopt%3DAbstract</link>
            <description>Authors: Kuphal S, Bosserhoff AK
    The Wnt/β-catenin pathway is involved in differentiation events during embryonic development and is further described as a pathway often participating in tumor formation when aberrantly activated. Molecular studies concentrating on colorectal cancer revealed mutations of apc, ctnnbi, btrc and tcf-4 genes which mimic Wnt stimulation. However, such mutations are rarely found during melanoma development. Therefore, we analyzed the β-catenin activity in this type of skin cancer. Interestingly, localization of β-catenin protein was basically cytoplasmic in melanomas in vivo, which was in clear contrast to findings in colon carcinoma. Congruently, the transcriptional activity of β-catenin regulating expression of β-catenin target genes was not observed ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4874218</comments>
            <pubDate>Sat, 28 May 2011 20:15:06 +0100</pubDate>
            <guid isPermaLink="false">4874218</guid>        </item>
        <item>
            <title>The anti-CD20 mAb LFB-R603 interrupts the dysregulated NF-κB/Snail/RKIP/PTEN resistance loop in B-NHL cells: Role in sensitization to TRAIL apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=4821277&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455568%26dopt%3DAbstract</link>
            <description>We examined several experimental designs for the biological anti-tumor activity of LFB-R603 as well as its sensitizing activity to apoptosis in resistant non-Hodgin's B-cell lymphoma (B-NHL) in comparison to rituximab. Treatment of the B-NHL cell line Ramos with LFB-R603 was not toxic at the concentrations used and induced cell aggregation following culture at 24 and 48 h similarly to rituximab. Hence, we hypothesized that LFB-R603 may signal the tumor cells and modify intracellular survival/anti-apoptotic pathways. Treatment of Ramos cells with LFB-R603 inhibited the constitutively active NF-κB survival pathway, followed by significant potentiation of TRAIL-mediated apoptosis. We examined the underlying molecular mechanism by which the LFB-R603-mediated NF-κB inhibition results in the r...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821277</comments>
            <pubDate>Sat, 14 May 2011 07:53:10 +0100</pubDate>
            <guid isPermaLink="false">4821277</guid>        </item>
        <item>
            <title>Expression of connective tissue growth factor (CTGF/CCN2) in breast cancer cells is associated with increased migration and angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=4821276&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455569%26dopt%3DAbstract</link>
            <description>Authors: Chien W, O'Kelly J, Lu D, Leiter A, Sohn J, Yin D, Karlan B, Vadgama J, Lyons KM, Koeffler HP
    Connective tissue growth factor (CTGF/CCN2) belongs to the CCN family of matricellular proteins, comprising Cyr61, CTGF, NovH and WISP1-3. The CCN proteins contain an N-terminal signal peptide followed by four conserved domains sharing sequence similarities with the insulin-like growth factor binding proteins, von Willebrand factor type C repeat, thrombospondin type 1 repeat, and a C-terminal growth factor cysteine knot domain. To investigate the role of CCN2 in breast cancer, we transfected MCF-7 cells with full-length CCN2, and with four mutant constructs in which one of the domains had been deleted. MCF-7 cells stably expressing full-length CCN2 demonstrated reduced cell proliferat...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821276</comments>
            <pubDate>Sat, 14 May 2011 07:52:53 +0100</pubDate>
            <guid isPermaLink="false">4821276</guid>        </item>
        <item>
            <title>Differential augmentative effects of buthionine sulfoximine and ascorbic acid in As2O3-induced ovarian cancer cell death: Oxidative stress-independent and -dependent cytotoxic potentiation.</title>
            <link>http://www.medworm.com/index.php?rid=4821275&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455570%26dopt%3DAbstract</link>
            <description>In this study, we attempted to enhance the cytotoxicity of As2O3 in ovarian cancer cells through manipulation of cellular glutathione (GSH) levels using either buthionine sulfoximine (BSO) or ascorbic acid (AA). Results from our studies showed that combinatorial therapies using As2O3 with either low dose BSO or only pharmacological doses of AA acted synergistically to enhance the cytotoxicity of As2O3 in ovarian tumor cells. With these regimens, therapeutic selectivity was observed with preferential killing of ovarian tumor cells over normal fibroblast controls. Furthermore, contrary to previous reports, enhancement of As2O3-mediated cell killing by these two agents was propagated through different effects. With BSO, apoptotic and non-apoptotic cell death enhancement were mediated through ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821275</comments>
            <pubDate>Sat, 14 May 2011 07:52:48 +0100</pubDate>
            <guid isPermaLink="false">4821275</guid>        </item>
        <item>
            <title>α3β1 integrin promotes radiation-induced migration of meningioma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4821274&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455571%26dopt%3DAbstract</link>
            <description>Authors: Gogineni VR, Nalla AK, Gupta R, Gujrati M, Klopfenstein JD, Mohanam S, Rao JS
    Cell motility is influenced by the microenvironment, signal transduction and cytoskeleton rearrangement. Cancer cells become resistant to these control mechanisms and gain the ability to move throughout the body and invade healthy tissues, which leads to metastatic disease. Integrins respond to context-dependent cues and promote cell migration and survival in cancer cells. In the present study, we analyzed the role of integrins in radiation-induced migration of meningioma cells. Migration and cell proliferation assays revealed that radiation treatment (7 Gy) significantly increased migration and decreased proliferation in two cell lines, IOMM-Lee and CH-157-MN. α3 and β1 integrins were overexpresse...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821274</comments>
            <pubDate>Sat, 14 May 2011 07:52:42 +0100</pubDate>
            <guid isPermaLink="false">4821274</guid>        </item>
        <item>
            <title>Effects of human leukocyte antigen (HLA)-DR engagement on melanoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4821273&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455572%26dopt%3DAbstract</link>
            <description>Authors: Barbieri G, Rimini E, Costa MA
    Melanoma cells often display constitutive expression of the major histocompatibility complex (MHC) class II molecules which is associated with a higher metastatic dissemination. The MHC class II molecules during T cell/ professional antigen-presenting cell (APC) interactions are localized, as signalling receptors, into membrane lipid rafts which are thought to be sites of signalling complex assembly. Therefore, with the aim of understanding the molecular mechanisms used by melanoma cells to frustrate an effective anti-tumour response we stimulated a MHC class II consti-tutive expressing melanoma cell line with a specific antibody that mimics the interaction of T-cell receptor (TCR) with class II molecules. In stimulated melanoma cells we showed t...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821273</comments>
            <pubDate>Sat, 14 May 2011 07:52:36 +0100</pubDate>
            <guid isPermaLink="false">4821273</guid>        </item>
        <item>
            <title>VEGF-A not Ang2 mediates endothelial-like differentiation of immature DCs by ERK1/2 signaling in the microenvironment of human colon adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4821272&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455573%26dopt%3DAbstract</link>
            <description>Authors: Lu J, Liu K, Zhao J, Zhao J, Ma J, Yang H, Huang Y, Qin Z, Bai R, Jiang L, Lv F, Li P, Yan W, Zhao M, Dong Z
    Endothelial-like differentiation of dendritic cells (DCs) is an interesting and significant phenomenon, which is worth further investigation. Here, we show that the tumor microenvironment derived from the supernatant of the SW620 human colon adenocarcinoma cell line and colon adenocarcinoma tissue homogenate can promote immature DCs (iDCs) to differentiate from the DC pathway toward endothelial cells, while the peri-carcinoma homogenate supernatant does not have this role. Inhibition of angiopoietin-2 (Ang2) in the supernatant by its antibody has no obvious influence on the endothelial-like differentiation. In contrast, inhibition of vascular endothelial growth factor-A...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821272</comments>
            <pubDate>Sat, 14 May 2011 07:52:31 +0100</pubDate>
            <guid isPermaLink="false">4821272</guid>        </item>
        <item>
            <title>IGF gene polymorphisms and breast cancer in African-American and Hispanic women.</title>
            <link>http://www.medworm.com/index.php?rid=4821271&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455574%26dopt%3DAbstract</link>
            <description>In this study, we investigated the association between gene polymorphisms along the IGF axis and breast cancer, including the IGF-1 (CA) dinucleotide repeat, IGFBP-3 A-202C single nucleotide polymorphism, and the 2-bp deletion and (AGG)n repeat polymorphisms in the IGF type 1 receptor (IGF-IR). A total of 654 subjects, including both African-American and Hispanic/Latino subjects, were screened for various gene polymorphisms. IGF gene polymorphism genotyping was performed by PCR-GeneScan and PCR-RFLP methods. Our results demonstrated a significant association between the non-19/non-19 IGF-1 (CA)n polymorphism and breast cancer (OR=1.75; 95% CI=1.07-2.88; P=0.027). Furthermore, absence of the wild-type-19 allele and alleles &amp;lt;(CA)19 were strongly associated with breast cancer (OR=1.82; 95%...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821271</comments>
            <pubDate>Sat, 14 May 2011 07:52:26 +0100</pubDate>
            <guid isPermaLink="false">4821271</guid>        </item>
        <item>
            <title>Up-regulation of insulin-like growth factor-binding protein 3 by 5-fluorouracil (5-FU) leads to the potent anti-proliferative effect of androgen deprivation therapy combined with 5-FU in human prostate cancer cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=4821270&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455575%26dopt%3DAbstract</link>
            <description>In this study, we investigated the synergistic mechanism of anti-androgen and 5-fluorouracil (5-FU) combination therapy against castration-resistant prostate cancer (CRPC). Four prostate cancer cell lines, LNCaP, 22Rv1, DU145 and PC3, were examined for their growth dependency on androgens and the insulin-like growth factor 1 (IGF1). We assessed the expression changes of certain growth factor receptors and regulating proteins when treated with 5-FU, and found that 5-FU increased the expression of the IGF-binding protein 3 (IGFBP3). Furthermore, 5-FU inhibited the phosphorylation of Akt and p70 S6K, while the knockdown of IGFBP3 reduced the levels of poly (ADP-ribose) polymerase cleaved by 5-FU in PC3 cells. Therefore, the up-regulation of IGFBP3 by 5-FU not only inhibits cell growth by redu...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821270</comments>
            <pubDate>Sat, 14 May 2011 07:52:20 +0100</pubDate>
            <guid isPermaLink="false">4821270</guid>        </item>
        <item>
            <title>Mechanisms of the apoptosis induced by CD176 antibody in human leukemic cells.</title>
            <link>http://www.medworm.com/index.php?rid=4821269&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455576%26dopt%3DAbstract</link>
            <description>In this study, we investigated the mechanisms of apoptosis induced by the CD176 antibody. We found that CD95 (FAS, APO-1) and the death receptor 4 (DR4) (TRAIL-R1) are co-expressed with CD176 on the surface of defined leukemic cells as observed by confocal microscopy and flow cytometry analyses. Further-more, CD95, CD45, CD43 and DR4 are carrier proteins of CD176 in hematopoietic cells recognized by means of sandwich solid-phase enzyme linked immunosorbent assay and co-immunoprecipitation. As shown by microarray analysis, 20 genes which are directly related to the execution, induction or positive regulation of apoptosis, were up-regulated after CD176 antibody treatment of the KG1 cell line. Nine differ-entially expressed genes observed in the microarray analysis were verified by quantitati...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821269</comments>
            <pubDate>Sat, 14 May 2011 07:52:15 +0100</pubDate>
            <guid isPermaLink="false">4821269</guid>        </item>
        <item>
            <title>Crude phenolic extracts from extra virgin olive oil circumvent de novo breast cancer resistance to HER1/HER2-targeting drugs by inducing GADD45-sensed cellular stress, G2/M arrest and hyperacetylation of Histone H3.</title>
            <link>http://www.medworm.com/index.php?rid=4821268&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455577%26dopt%3DAbstract</link>
            <description>Authors: Oliveras-Ferraros C, Fernández-Arroyo S, Vazquez-Martin A, Lozano-Sánchez J, Cufí S, Joven J, Micol V, Fernández-Gutiérrez A, Segura-Carretero A, Menendez JA
    Characterization of the molecular function of complex phenols naturally present in extra virgin olive oil (EVOO) against the HER2-gene amplified JIMT-1 cell line, a unique breast cancer model that inherently exhibits cross-resistance to multiple HER1/2-targeted drugs including trastuzumab, gefitinib, erlotinib and lapatinib, may underscore innovative cancer molecules with novel therapeutic targets because they should efficiently circumvent de novo resistance to HER1/2 inhibitors in order to elicit tumoricidal effects. We identified pivotal signaling pathways associated with the efficacy of crude phenolic extracts (PE...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821268</comments>
            <pubDate>Sat, 14 May 2011 07:52:07 +0100</pubDate>
            <guid isPermaLink="false">4821268</guid>        </item>
        <item>
            <title>Clinical significance of expression of Hint1 and potential epigenetic mechanism in gastric cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4821267&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21468541%26dopt%3DAbstract</link>
            <description>Authors: Huang H, Wei X, Su X, Qiao F, Xu Z, Gu D, Fan H, Chen J
    HINT1, a member of the evolutionary highly conserved HIT protein superfamily, is ubiquitously expressed in diverse species including mammalian tissues. Accumulating evidence shows that HINT1 is a haploinsufficient tumor suppressor. In the present study, we explored possible correlations between the expression level of HINT1 and clinicopathological features in tissues from gastric cancer (GC) patients. Decreased expression of HINT1 detected by qPCR and Western blotting in tumor tissues was found in 58.82 and 39.2% of the patients, respectively. Significantly reduced expression of HINT1 was found in poorly differentiated tumor tissues (p=0.027). Environmental interference (either H. pylori or EBV infection) (p=0.005) was as...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821267</comments>
            <pubDate>Sat, 14 May 2011 07:52:01 +0100</pubDate>
            <guid isPermaLink="false">4821267</guid>        </item>
        <item>
            <title>p120-catenin isoform 3 regulates subcellular localization of Kaiso and promotes invasion in lung cancer cells via a phosphorylation-dependent mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=4821266&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21468542%26dopt%3DAbstract</link>
            <description>Authors: Zhang PX, Wang Y, Liu Y, Jiang GY, Li QC, Wang EH
    p120-catenin regulates E-cadherin stability at the plasma membrane as well as Rho GTPase activity in the cyto-plasm, and also interacts with the transcriptional repressor, Kaiso, in the nucleus. However, the role of different isoforms and the phosphorylated state of p120-catenin in the nucleus is poorly understood. In the present study, we show that p120-catenin isoform 3 interacts with Kaiso in lung cancer cells by immunoprecipitation. Nuclear-cytoplasmic extraction and immunofluoresence confirmed that Kaiso shuttled out of the nucleus via p120-catenin isoform 3. The cytoplasmic enrichment of Kaiso by p120-catenin isoform 3 was abolished due to the inhibition of chromosomal region maintenance-dependent nuclear export via lepto...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821266</comments>
            <pubDate>Sat, 14 May 2011 07:51:55 +0100</pubDate>
            <guid isPermaLink="false">4821266</guid>        </item>
        <item>
            <title>Suppression of growth and invasive behavior of human prostate cancer cells by ProstaCaidTM: Mechanism of activity.</title>
            <link>http://www.medworm.com/index.php?rid=4821265&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21468543%26dopt%3DAbstract</link>
            <description>In conclusion, the dietary supplement PC is a promising natural complex with the potency to inhibit invasive human prostate cancer.
    PMID: 21468543 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821265</comments>
            <pubDate>Sat, 14 May 2011 07:51:46 +0100</pubDate>
            <guid isPermaLink="false">4821265</guid>        </item>
        <item>
            <title>Opposite regulation of epithelial-to-mesenchymal transition and cell invasiveness by periostin between prostate and bladder cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4821264&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21468544%26dopt%3DAbstract</link>
            <description>Authors: Kim CJ, Sakamoto K, Tambe Y, Inoue H
    We previously showed that periostin expression is downregulated in human bladder cancer tissues and that ectopic expression of periostin suppresses the invasiveness of bladder cancer cells. However, in most other human cancers studied, the expression of periostin promotes cell invasiveness. In the present study, we investigated the regulation of the epithelial-to-mesenchymal transition (EMT) and cell invasiveness by periostin in bladder and prostate cancer cell lines, and found opposite regulation of EMT and cell invasiveness by periostin. Periostin upregulated E-cadherin expression in bladder cancer cells but downregulated it in prostate cancer cells. Periostin suppressed cell invasiveness in bladder cancer cells but promoted it in prostat...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821264</comments>
            <pubDate>Sat, 14 May 2011 07:51:42 +0100</pubDate>
            <guid isPermaLink="false">4821264</guid>        </item>
        <item>
            <title>STAT3-targeting RNA interference inhibits pancreatic cancer angiogenesis in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=4821263&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21479358%26dopt%3DAbstract</link>
            <description>The objective of this study was to evaluate the potential use of RNA interference (RNAi) to knock down the STAT3 gene and the effect on angiogenesis of human pancreatic cancer cells in vitro and in vivo. We stably inhibited the expression of STAT3 and phosphorylated STAT3 (p-STAT3) using RNAi in the SW1990 pancreatic cancer cell line. Furthermore, RNAi for STAT3 inhibited STAT3-induced HUVEC cell migration and cell proliferation, and significantly suppressed the levels of secreted vascular endothelial growth factor (VEGF) and matrix metalloproteinases-2 (MMP-2) of SW1990 cells. In vivo experiments showed that RNAi for STAT3 significantly suppressed tumor growth and angiogenesis of SW1990 cells. Furthermore, silencing the STAT3 gene in SW1990 cells by RNAi also led to a decrease of VEGF and...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821263</comments>
            <pubDate>Sat, 14 May 2011 07:51:38 +0100</pubDate>
            <guid isPermaLink="false">4821263</guid>        </item>
        <item>
            <title>Leuprorelin acetate affects adhesion molecule expression in human prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4821262&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21479359%26dopt%3DAbstract</link>
            <description>Authors: Angelucci C, Lama G, Iacopino F, Sica G
    Reduced cell-cell adhesion allows malignant epithelial cells to invade the basal membrane and penetrate the stroma. This implies the potential of the cells to escape from the primary tumor as well as spreading ability. Herein, we investigated the effects of leuprorelin acetate (LA), a GnRH agonistic analogue, alone or in combination with dihydrotestosterone (DHT), on the expression of molecules involved in cell adhesion (E-cadherin, N-cadherin, α-, β- and γ-catenin) or in migration/invasion (c-met, CD44v6 and caveolin-1) in androgen-sensitive (LNCaP) and -insensitive (PC-3) prostate cancer (CaP) cells. We demonstrated by immunoblotting that, in LNCaP cells, molecules present in the adherens junctions (E-cadherin, α-, β- and γ-caten...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821262</comments>
            <pubDate>Sat, 14 May 2011 07:51:34 +0100</pubDate>
            <guid isPermaLink="false">4821262</guid>        </item>
        <item>
            <title>A demethylating agent enhances chemosensitivity to vinblastine in a xenograft model of renal cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4821261&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21479360%26dopt%3DAbstract</link>
            <description>In this study, we investigated the combined effect of Aza and VBL in a Caki-1 xenograft model and in other RCC cell lines in vitro. In the xenograft model, tumor volume and weight were significantly suppressed in the co-treatment group, compared to the control, and the expressions of P-glycoprotein, Bcl-2 and cyclin B1 were reduced. Thus, this combined effect could be mediated by the accumulation of intracellular VBL and the enhancement of apoptosis and cell cycle arrest. More-over, the cytotoxicity of VBL was enhanced in vitro in three RCC cell lines by Aza treatment. These findings suggest that the combination treatment with Aza and VBL is effective against RCC.
    PMID: 21479360 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821261</comments>
            <pubDate>Sat, 14 May 2011 07:51:30 +0100</pubDate>
            <guid isPermaLink="false">4821261</guid>        </item>
        <item>
            <title>FLT-PET may not be a reliable indicator of therapeutic response in p53-null malignancy.</title>
            <link>http://www.medworm.com/index.php?rid=4821242&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537838%26dopt%3DAbstract</link>
            <description>We examined the therapeutic predictive value of FLT-PET and FDG-PET using CALU-6, a human, p53-null, non-small cell lung cancer cell line with comparison of combined targeted therapy, TRAIL and sorafenib, versus combined conventional chemotherapy, docetaxel and cisplatin. CALU-6 tumor-bearing nu/nu mice (n=46) were evaluated in 3 therapeutic trials measuring FLT and FDG prediction of tumor response at 72 h following initiation of daily combination therapy with targeted agents, TRAIL (200 µg i.v.) and sorafenib (30 mg/kg i.p.) and compared to conventional chemotherapeutics cisplatin (3 mg/kg i.p.) and docetaxel (7.5 mg/kg i.p.). PET imaging response was compared to morphological and histological indicators of therapeutic response, including decreased vascu-larity (in vivo AngioSense im...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821242</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821242</guid>        </item>
        <item>
            <title>Endosialin is expressed in high grade and advanced sarcomas: Evidence from clinical specimens and preclinical modeling.</title>
            <link>http://www.medworm.com/index.php?rid=4821241&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537839%26dopt%3DAbstract</link>
            <description>Authors: Rouleau C, Smale R, Fu YS, Hui G, Wang F, Hutto E, Fogle R, Jones CM, Krumbholz R, Roth S, Curiel M, Ren Y, Bagley RG, Wallar G, Miller G, Schmid S, Horten B, Teicher BA
    We previously surveyed the expression of endosialin/ CD248/TEM-1 by immunohistochemistry in human clinical specimens of sarcomas and documented expression in tumor cells, stromal cells and vasculature. In the present study, we completed a retrospective analysis of the diagnostic reports available for these same samples in order to identify high-grade and metastatic disease. Our results show that endosialin can be detected in advanced disease. We screened human sarcoma cell lines in vitro for endosialin expression and developed preclinical human xenograft models of disseminated sarcoma. We found that 22 out of ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821241</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821241</guid>        </item>
        <item>
            <title>Methylation-related mutations in the BRCA1 promoter in peripheral blood cells from cancer-free women.</title>
            <link>http://www.medworm.com/index.php?rid=4821240&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537840%26dopt%3DAbstract</link>
            <description>Authors: Al-Moghrabi N, Al-Qasem AJ, Aboussekhra A
    Early-onset breast cancer is one of the most common malignancies and causes of death among young women, and its incidence is increasing. In the present study, we aimed to investigate the epigenetic modifications of the breast cancer type 1 susceptibility gene (BRCA1) in breast tissues and blood cells derived from women with breast cancer and women without breast cancer. BRCA1 promoter methylation was examined by methylation-specific PCR in 47 breast cancer tissues and in peripheral blood cells derived from 7 breast cancer patients and 73 healthy women. Subse-quently, the methylation status of the BRCA1 promoter was confirmed and analyzed at high resolution by sodium bisulfite genomic sequencing. BRCA1 promoter methylation was detected ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821240</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821240</guid>        </item>
        <item>
            <title>Vandetanib inhibits both VEGFR-2 and EGFR signalling at clinically relevant drug levels in preclinical models of human cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4821239&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537841%26dopt%3DAbstract</link>
            <description>Authors: Brave SR, Odedra R, James NH, Smith NR, Marshall GB, Acheson KL, Baker D, Howard Z, Jackson L, Ratcliffe K, Wainwright A, Lovick SC, Hickinson DM, Wilkinson RW, Barry ST, Speake G, Ryan AJ
    Vandetanib is a multi-targeted receptor tyrosine kinase inhibitor that is in clinical development for the treatment of solid tumours. This preclinical study examined the inhibition of two key signalling pathways (VEGFR-2, EGFR) at drug concentrations similar to those achieved in the clinic, and their contribution to direct and indirect antitumour effects of vandetanib. For in vitro studies, receptor phosphorylation was assessed by Western blotting and ELISA, cell proliferation was assessed using a cell viability endpoint, and effects on cell cycle determined using flow cytometry. For in vivo...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821239</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821239</guid>        </item>
        <item>
            <title>Urothelial cancer cell response to combination therapy of gemcitabine and TRAIL.</title>
            <link>http://www.medworm.com/index.php?rid=4821238&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537842%26dopt%3DAbstract</link>
            <description>Authors: Moibi JA, Mak AL, Sun B, Moore RB
    High-risk superficial urothelial carcinoma of the bladder (UCB) is commonly treated with intravesical bacillus Calmette-Guerin (BCG), but with significant side effects. We recently showed that the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) exhibited high therapeutic potential against UCB cells and with only limited toxic effects in normal cells. However, many cancer cells are refractory to TRAIL during monotherapy. Therefore, our experimental aim was to develop combinatorial approaches with other pro- apoptotic agents to reactivate apoptosis in resistant phenotypes. We demonstrate that UCB cells varied in their response to TRAIL, and the effect was caspase-dependent (reduced or abrogated by pre-incubation of cells with ca...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821238</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821238</guid>        </item>
        <item>
            <title>Monoamine carboxylate transporters are involved in BI-1-associated cancer metastasis in HT1080 colon fibrosarcoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4821237&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537843%26dopt%3DAbstract</link>
            <description>In this study, ion transporters such as sodium hydrogen exchangers (NHE) and monoamine carboxylate transporters (MCTs) were studied in BI-1-overexpressing HT1080 cells (BI-1 cells). The extracellular pH became acidic as culture time of BI-1 cells increased, while intracellular pH stayed relatively stable at pH 7.2. The expression of MCTs increased in BI-1 cells as culture time passed. 5-(N-ethyl-N-isopropyl) amiloride or dimethylamiloride, NHE inhibitor, abrogated the elevated MCT expression, indicating that MCT followed NHE activation. An MCT inhibitor, lonidamine, regulated the acidification of extracellular pH, also inhibiting both increased cancer cell migration and infiltration and MMP2/9 activity. The inhibition of either NHE or MCT affected the intracellular pH, leading to a severel...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821237</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821237</guid>        </item>
        <item>
            <title>Autophagy and cell death signaling following dietary sulforaphane act independently of each other and require oxidative stress in pancreatic cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4821236&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537844%26dopt%3DAbstract</link>
            <description>Authors: Naumann P, Fortunato F, Zentgraf H, Büchler MW, Herr I, Werner J
    The broccoli isothiocyanate, sulforaphane (SFN), was recently identified as being capable of eliminating highly therapy-resistant pancreatic carcinoma (PC) cells without inducing toxic side effects. While SFN has been shown to stimulate autophagy or 'self-eating', it is unclear whether this catabolic process is a pro- or anti-tumorigenic response. To investigate the role of autophagy in SFN-induced cell death, established PC cell lines were treated with SFN, and the induction of autophagy was evaluated by detecting the abundance of autophagic vesicles by electron microscopy, the increase in converted LC3-II by Western blot analysis and the autophagosome puncta of GFP-LC3 by immunofluorescence. SFN-induced autoph...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821236</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821236</guid>        </item>
        <item>
            <title>Human umbilical cord blood-derived mesenchymal stem cells improve glucose homeostasis in rats with liver cirrhosis.</title>
            <link>http://www.medworm.com/index.php?rid=4821245&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537835%26dopt%3DAbstract</link>
            <description>Authors: Jung KH, Uhm YK, Lim YJ, Yim SV
    Disturbance of glucose metabolism is a common feature in liver cirrhosis which is associated with insulin resistance and is an established risk factor for disease progression and survival in patients with chronic liver diseases. We investigated whether umbilical cord blood-derived mesenchymal stem cells (HMSCs) have an effect on the expression of molecules responsible for glucose utilization and hepatic gluconeogenesis, focusing on the insulin signaling pathway in rats with liver cirrhosis. Rats received a dose of CCl4 (100 µl/100 g 4:1 in corn oil) thrice-weekly. HMSCs were infused at 4 weeks after induction of liver cirrhosis by CCl4. Infusion of HMSCs improved insulin resistance which was associated with increased glucose levels and decrease...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821245</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821245</guid>        </item>
        <item>
            <title>Artesunate enhances TRAIL-induced apoptosis in human cervical carcinoma cells through inhibition of the NF-κB and PI3K/Akt signaling pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4821244&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537836%26dopt%3DAbstract</link>
            <description>Authors: Thanaketpaisarn O, Waiwut P, Sakurai H, Saiki I
    Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis and kills cancer cells with little or no adverse effects on normal cells. TRAIL is relatively safe for clinical applications. However, TRAIL resistance is widely found in cancer cells leading to limitations in utilizing TRAIL as a therapeutic agent for cancer treatment. Recently, artesunate, an effective and safe anti-malarial drug, was also described as a promising candidate for cancer therapy. It would be of importance to determine whether combination treatment of TRAIL together with artesunate could overcome drug-resistance of tumors. Here, we demonstrate the first evidence that artesunate effectively enhances TRAIL-mediated cytotoxic...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821244</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821244</guid>        </item>
        <item>
            <title>FBXO31 determines poor prognosis in esophageal squamous cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4821243&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21537837%26dopt%3DAbstract</link>
            <description>In this study, we clarified the clinical significance of FBXO31 and characterized the association between cyclin D1 and FBXO31 in ESCC cases. Total RNA was extracted from tumor tissues obtained from 68 ESCC patients who underwent surgical resection. FBXO31 expression levels were determined by quantitative RT-PCR, and both FBXO31 and cyclin D1 protein expression and localization were evaluated by immunohistochemistry (IHC). Furthermore, using CGH and gene expression array data of another subset, we validated the association between cyclin D1 genomic amplification and FBXO31 expression levels. Higher FBXO31 expression levels significantly correlated with depth of tumor invasion and clinical stage (P&amp;lt;0.05). In addition, the FBXO31 high expression group showed a significantly poorer prognos...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821243</comments>
            <pubDate>Wed, 27 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821243</guid>        </item>
        <item>
            <title>Antitumor activities of JTP-74057 (GSK1120212), a novel MEK1/2 inhibitor, on colorectal cancer cell lines in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=4821246&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21523318%26dopt%3DAbstract</link>
            <description>Authors: Yamaguchi T, Kakefuda R, Tajima N, Sowa Y, Sakai T
    The MAPK pathway is one of the most important pathways for novel anticancer drug development. We performed high-throughput screening for compounds that induce expression of p15INK4b, and identified JTP-74057 (GSK1120212), which is being evaluated in ongoing phase I, II and III clinical trials. We characterized its antitumor activities in vitro and in vivo. JTP-74057 strongly inhibited MEK1/2 kinase activities, but did not inhibit another 98 kinase activities. Treatment by JTP-74057 resulted in growth inhibition accompanied with upregulation of p15INK4b and/or p27KIP1 in most of the colorectal cancer cell lines tested. Daily oral administration of JTP-74057 for 14 days suppressed tumor growth of HT-29 and COLO205 xenografts ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821246</comments>
            <pubDate>Mon, 25 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821246</guid>        </item>
        <item>
            <title>Synergistic cytotoxicity of N-methyl-N'-nitro-N-nitrosoguanidine and absence of poly(ADP-ribose) glycohydrolase involves chromatin decondensation.</title>
            <link>http://www.medworm.com/index.php?rid=4821248&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21519789%26dopt%3DAbstract</link>
            <description>Authors: Zhou Y, Feng X, Koh DW
    DNA-alkylating agents in combination with poly (ADP-ribose) (PAR) synthesis inhibitors are a promising treatment for cancer. In search of other efficacious alternatives, we hypothesized that the absence of poly(ADP-ribose) glycohydrolase (PARG), which leads to the inhibition of PAR hydrolysis, would lead to increased DNA alkylation after treatment with low doses of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). At a sublethal dose, MNNG shows synergistic cytotoxicity in PARG-null embryonic trophoblast stem (TS) cells. The PAR modifications of histone H1 and histone H2B are much more pronounced in PARG null-TS cells exposed to MNNG, suggesting their relevance in the efficacy of this combination therapy. Because the PAR modification of these chromatin bindin...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821248</comments>
            <pubDate>Wed, 20 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821248</guid>        </item>
        <item>
            <title>Histone deacetylase inhibitors, valproic acid and trichostatin-A induce apoptosis and affect acetylation status of p53 in ERG-positive prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4821247&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21519790%26dopt%3DAbstract</link>
            <description>In this study, we tested the effect of the HDAC inhibitors valproic acid (VPA) and trichostatin-A (TSA) on ERG-positive prostate cancer cells (VCaP). We found that VPA and TSA induce apoptosis, upregulate p21/Waf1/CIP1, repress TMPRSS2-ERG expression and affect acetylation status of p53 in VCaP cells. These results suggest that HDAC inhibitors might restore HAT activity through two different ways: by inhibiting HDAC activity and by repressing HAT targeting oncoproteins such as ERG.
    PMID: 21519790 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821247</comments>
            <pubDate>Wed, 20 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821247</guid>        </item>
        <item>
            <title>miR-218 on the genomic loss region of chromosome 4p15.31 functions as a tumor suppressor in bladder cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4821249&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21519788%26dopt%3DAbstract</link>
            <description>Authors: Tatarano S, Chiyomaru T, Kawakami K, Enokida H, Yoshino H, Hidaka H, Yamasaki T, Kawahara K, Nishiyama K, Seki N, Nakagawa M
    Growing evidence suggests that microRNAs (miRNAs) are aberrantly expressed in many human cancers, and that they play significant roles in carcinogenesis and cancer progression. The identification of tumor suppressive miRNAs and their target genes could provide new insights into the mechanism of carcinogenesis. However, the genetic or epigenetic regulations of these miRNAs have not yet been fully elucidated in bladder cancer (BC). Chromosomal alter-ations of cancer cells give us important information for the identification of tumor suppressor genes. Our miRNA array-comparative genomic hybridization (CGH) analysis showed several miRNAs to be candidate tumo...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821249</comments>
            <pubDate>Tue, 19 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821249</guid>        </item>
        <item>
            <title>Substrate optimization and clinical validation of reporter peptides for MS-based protease profiling in serum specimens: A new approach for diagnosis of malignant disease.</title>
            <link>http://www.medworm.com/index.php?rid=4821252&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503574%26dopt%3DAbstract</link>
            <description>In this study, we describe the systematic optimization of a synthetic peptide substrate using a positional scanning synthetic combinatorial library (PS-SCL) approach. The initial reporter peptide (RP) comprises of the cleavage site, WKPYDAAD, that is part of the coagulation factor X, the natural substrate of the tumor-associated cysteine protease cancer procoagulant (EC 3.4.22.26). Specifically, the amino acid substitution of aspartatic acid (D) in position P1' against asparagine (N) improved the processing of respective RPs in serum specimens from patients with colorectal tumors compared to healthy controls. Proteolytic fragments of RPs accumulated during prolonged incubation with serum specimens and were quantified with matrix-assisted laser desorption/ionization time-of-ﬂight mass spe...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821252</comments>
            <pubDate>Sun, 17 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821252</guid>        </item>
        <item>
            <title>Human complement factor H is a novel diagnostic marker for lung adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4821251&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503575%26dopt%3DAbstract</link>
            <description>In this study, we investigated the role of CFH in human lung cancer. Expression of CFH was analyzed in lung cancer cell lines by RT-PCR, Western blotting and immunofluorescence. In primary lung tumors, the protein expression of CFH was evaluated by immunohistochemistry (IHC) on tissue microarray (TMA). Binding of CFH to lung cancer cells was detected by flow cytometry. mRNA expression of CFH was detected in 6 out of 10 non-small cell lung cancer (NSCLC) cell lines, but in none of the small cell lung cancer (SCLC) cell lines. In line with Western blotting, immunofluorescence analysis demonstrated CFH protein expression in 3 NSCLC cell lines, and the immunoreaction was mainly associated with cell cytoplasm and membrane. In primary lung tumors, 54 out of 101 samples exhibited high expression ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821251</comments>
            <pubDate>Sun, 17 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821251</guid>        </item>
        <item>
            <title>Sesamin induces autophagy in colon cancer cells by reducing tyrosine phosphorylation of EphA1 and EphB2.</title>
            <link>http://www.medworm.com/index.php?rid=4821250&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503576%26dopt%3DAbstract</link>
            <description>Authors: Tanabe H, Kuribayashi K, Tsuji N, Tanaka M, Kobayashi D, Watanabe N
    Receptor tyrosine kinase EphB2 and autophagic machinery are known as tumor suppressors; however, the connection remains to be elucidated. Here, we show the link between EphB2 and autophagy. Sesamin, a major lignan in sesame oil, induced autophagy in the human colon cancer cell lines HT29 and LS180, as shown by electron microscopy, as well as Western blotting and immunofluorescence imaging using an anti-LC3 antibody. Receptor tyrosine kinase array analysis revealed that sesamin treatment increased the levels of unphosphorylated -EphA1 and -EphB2 in HT29 cells. Silencing of EphA1 and EphB2 blocked sesamin-induced autophagy as well as sesamin-induced loss of cell viability. These results show that EphA1 and EphB2...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821250</comments>
            <pubDate>Sun, 17 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821250</guid>        </item>
        <item>
            <title>MALAT-1: A long non-coding RNA and its important 3' end functional motif in colorectal cancer metastasis.</title>
            <link>http://www.medworm.com/index.php?rid=4821254&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503572%26dopt%3DAbstract</link>
            <description>In this study, we analyzed the MALAT-1 gene in five fragments. We employed the sequencing process to identify MALAT-1 mutations in the following types of samples: CRC cells (SW620, SW480), normal colorectal tissues, and primary CRC tissues. We were successful in detecting the following mutations: fragment 5434 nt-6951 nt of the MALAT-1 was mutated in SW620 cells, while fragments 5434 nt-6951 nt and 6918 nt-8441 nt of MALAT-1 were mutated in SW480 cancer cells and primary CRC tissues. We over-expressed five fragments of MALAT-1 in the CRC cell line SW480; simultaneously ensuring that MALAT-1 had low expression. Our data illustrated that one of the 5 fragments (6918 nt-8441 nt) located at the 3' end of MALAT-1 plays a pivotal role in the biological processes of cell proliferation, migration ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821254</comments>
            <pubDate>Thu, 14 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821254</guid>        </item>
        <item>
            <title>Catechol estrogens as biomarkers for mammary gland cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4821253&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503573%26dopt%3DAbstract</link>
            <description>Authors: Calaf GM, Garrido F
    The origin of human tumors has been attributed to the exposure to several environmental chemicals and implicated in the increase of incidence in breast cancer. Progression of breast cancer follows a complex multistep process that seems to depend on various exogenous and endogenous factors. The aim of this study was to examine the effects of the organo-phosphorous pesticide malathion in the presence of estrogen on neoplastic transformation of rat mammary glands. Virgin female rats were sacrificed after 30, 124 and 240 days of 5-day injections twice a day. There were four groups: i) control, ii) malathion (22 mg/100 g body weight, BW), iii) 17β-estradiol (30 µg/100 g BW) and iv) combination of both. Progressive alterations in ducts were observed by the eff...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821253</comments>
            <pubDate>Thu, 14 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821253</guid>        </item>
        <item>
            <title>Overexpression of α1,6-fucosyltransferase in hepatoma enhances expression of Golgi phosphoprotein 2 in a fucosylation-independent manner.</title>
            <link>http://www.medworm.com/index.php?rid=4821256&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503570%26dopt%3DAbstract</link>
            <description>Authors: Kawamoto S, Moriwaki K, Nakagawa T, Terao M, Shinzaki S, Yamane-Ohnuki N, Satoh M, Mehta AS, Block TM, Miyoshi E
    Golgi phosphoprotein 2 (GP73) is a type II Golgi protein, which was found on examination of the fucosylated proteome as a potential tumor marker for hepatocellular carcinoma (HCC). The serum levels of both total and fucosylated GP73 were increased in the sera of patients with HCC. Fucosylation is one of the most important oligosaccharide modifications involved in cancer and is catalyzed by α1,6-fucosyltransferase (Fut8). In the present study, we investigated the effect of Fut8 overexpression on GP73 production in the human hepatoma cell line Hep3B. The Fut8 expression vector was transfected into Hep3B cells and the expression of GP73 was investigated by Western blo...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821256</comments>
            <pubDate>Wed, 13 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821256</guid>        </item>
        <item>
            <title>The level of secretory leukocyte protease inhibitor is decreased in metastatic head and neck squamous cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4821255&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21503571%26dopt%3DAbstract</link>
            <description>Authors: Cordes C, Häsler R, Werner C, Görögh T, Röcken C, Hebebrand L, Kast WM, Hoffmann M, Schreiber S, Ambrosch P
    Head and neck squamous cell carcinomas (HNSCC) represent the sixth largest group among all human malignancies. However, the exact molecular mechanisms inducing the genesis and the progression of metastasis in these tumors are poorly understood. The identification of molecular alterations involved in metastasis of HNSCC might influence the value of clinical diagnostics, impact therapy strategies and finally improve the prognosis of the patients. The purpose of this study was to identify clinically relevant alterations at the transcriptional and translational levels, when comparing metastatic (N+) and non-metastatic (N0) primary HNSCC. Three transcripts HERPUD1, SLPI a...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821255</comments>
            <pubDate>Wed, 13 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821255</guid>        </item>
        <item>
            <title>Bone metastases detection by circulating biomarkers: OPG and RANK-L.</title>
            <link>http://www.medworm.com/index.php?rid=4821260&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491082%26dopt%3DAbstract</link>
            <description>Authors: Mercatali L, Ibrahim T, Sacanna E, Flamini E, Scarpi E, Calistri D, Ricci M, Serra P, Ricci R, Zoli W, Kang Y, Amadori D
    Osteoprotegerin (OPG) is a decoy receptor of the receptor activator of nuclear factor-κB ligand (RANK-L) and plays an important role in the formation of metastatic bone lesions. We evaluated the usefulness of circulating OPG and RANK-L for the detection of bone metastases. We enrolled 143 individuals in the study: 30 healthy donors (HD) and 113 breast cancer patients. Among patients, 49 had no evidence of disease (NEDP), 54 had bone metastases (BMP) at first diagnosis, and 10 had visceral metastases (VMP). Both transcripts were determined in peripheral blood samples using quantitative PCR. Receiver operating characteristic (ROC) curve analysis was used to c...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821260</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821260</guid>        </item>
        <item>
            <title>Ultraviolet exposure of melanoma cells induces fibroblast activation protein-α in fibroblasts: Implications for melanoma invasion.</title>
            <link>http://www.medworm.com/index.php?rid=4821259&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491083%26dopt%3DAbstract</link>
            <description>We examined the effect of UVR on FAP-α expression in melanocytes, keratinocytes and fibroblasts from the skin and in melanoma cells. UVR induces upregulation of FAP-α in fibroblasts, melanocytes and primary melanoma cells (PM) whereas keratinocytes and metastatic melanoma cells remained FAP-α negative. UVA and UVB stimulated FAP-α-driven migration and invasion in fibroblasts, melanocytes and PM. In co-culture systems UVR of melanocytes, PM and cells from regional metastases upregulated FAP-α in fibroblasts but only supernatants from non-irradiated PM were able to induce FAP-α in fibroblasts. Further, UV-radiated melanocytes and PM significantly increased FAP-α expression in fibroblasts through secretory crosstalk via Wnt5a, PDGF-BB and TGF-β1. Moreover, UV radiated melanocytes and ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821259</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821259</guid>        </item>
        <item>
            <title>Mode of action of trifluorothymidine (TFT) against DNA replication and repair enzymes.</title>
            <link>http://www.medworm.com/index.php?rid=4821258&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491084%26dopt%3DAbstract</link>
            <description>Authors: Suzuki N, Emura T, Fukushima M
    Trifluorothymidine (TFT) is well known to be converted to TFT-monophosphate by thymidine kinase and to inhibit thymidylate synthase. In addition, TFT-triphosphate (TFT-TP) is also incorporated into DNA, resulting in cytocidal effects. However, the precise mechanism of TFT-induced DNA damage is still unclear. Therefore, we investigated the modes of action of TFT against DNA replication and repair enzymes, as compared with those of 5FU and FdUrd. When HeLa cells were treated with TFT at a concentration of 1 µM (IC50 value), the concentration of TFT in the DNA was calculated as 62.2±0.9 pmol/1x106 cells for 4 h. On the other hand, following treatment of the cells with FdUrd (0.5 µM) and 5FU (10 µM) at their IC50 doses, the drug concentrations in...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821258</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821258</guid>        </item>
        <item>
            <title>Lentivirally engineered dendritic cells activate AFP-specific T cells which inhibit hepatocellular carcinoma growth in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=4821257&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21491085%26dopt%3DAbstract</link>
            <description>This study supports the superiority of a full-length antigen lentivirus-based DCs vaccine strategy over peptides, and provides new insight into the design of DCs-based vaccines.
    PMID: 21491085 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4821257</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4821257</guid>        </item>
        <item>
            <title>Identification of ETS-1 target genes in human fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=4659666&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424123%26dopt%3DAbstract</link>
            <description>In this study we investigated the role of Ets-1 in the tumour stroma. It is well known that ets-1 expression in fibroblasts - one of the main components of the tumour stroma - can be induced by basic fibroblast growth factor (bFGF). We applied suppression subtractive hybridization (SSH) to identify genes that are differentially expressed between bFGF stimulated wild-type fibroblasts and fibroblasts with reduced Ets-1 expression. We selected clones up- or down-regulated in bFGF stimulated wild-type fibroblasts using SSH and functionally characterized them by reference to public databases using NCBI BLAST tools. Expression levels of genes corresponding to subtracted clones were analyzed using RT-PCR. Known genes were associated with diverse functions; novel Ets-1 regulated genes identified b...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659666</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659666</guid>        </item>
        <item>
            <title>Inhibition of the p38 MAPK pathway sensitises human colon cancer cells to 5-fluorouracil treatment.</title>
            <link>http://www.medworm.com/index.php?rid=4659665&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424124%26dopt%3DAbstract</link>
            <description>This study assessed whether the p38 MAPK pathway is involved in 5-FU resistance in colorectal cancer cells. 5-FU only or 5-FU combined with a p38 MAPK pathway inhibitor (SB203580) was used to treat 5-FU-resistant colorectal cancer cells. The effect of the treatment on cell viability, death and caspase activities was assessed. Western blotting was used to investigate the responses of apoptosis-related proteins following the treatment. Results showed that p38 MAPK inhibitor significantly increased colorectal cancer cell sensitivity to 5-FU. SB203580 in combination with 5-FU significantly reduced cell viability (P&amp;lt;0.01), and increased cell death and cellular caspase activity (P&amp;lt;0.01). Western blotting data revealed that SB203580 sensitises cancer cells to 5-FU due to an increase in Bax ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659665</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659665</guid>        </item>
        <item>
            <title>Role of aquaporin-4 in the regulation of migration and invasion of human glioma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4659664&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424125%26dopt%3DAbstract</link>
            <description>Authors: Ding T, Ma Y, Li W, Liu X, Ying G, Fu L, Gu F
    Glioblastoma is the most aggressive form of primary brain tumor with a tendency to invade surrounding healthy brain tissues, rendering tumors of this type largely incurable. Aquaporin-4 (AQP4) is a key molecule involved in maintaining water and ion homeostasis in the central nervous system and has been recently reported to play a role in cell migration in addition to its well-known function in brain edema. Increased AQP4 expression has been demonstrated in glioblastoma multiforme (GBM), suggesting that it is also involved in malignant brain tumors. Here, we identify a novel role for aquaporin-4 in glioblastoma cell migration and invasion. In the present study, we used small-interference RNA technology and a pharmacological inhibito...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659664</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659664</guid>        </item>
        <item>
            <title>Diallyl sulfide induces cell cycle arrest and apoptosis in HeLa human cervical cancer cells through the p53, caspase- and mitochondria-dependent pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4659673&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424116%26dopt%3DAbstract</link>
            <description>In conclusion, DAS induced G0/G1 cell cycle arrest and apoptosis in HeLa cells through caspase- and mitochondria and p53 pathways providing further understanding of the molecular mechanisms of DAS action in cervical cancer. This study, therefore, revealed that DAS significantly inhibits the growth and induces apoptosis of human cervical cancer HeLa cells in vitro.
    PMID: 21424116 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659673</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659673</guid>        </item>
        <item>
            <title>Epigenetic regulation of proMMP-1 expression in the HT1080 human fibrosarcoma cell line.</title>
            <link>http://www.medworm.com/index.php?rid=4659672&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424117%26dopt%3DAbstract</link>
            <description>Authors: Poplineau M, Dufer J, Antonicelli F, Trussardi-Regnier A
    The matrix metalloproteinase (MMP) family members play an important role in various physiological and pathological processes. Although MMP-1 (collagenase-1) has been shown to be involved in tumor invasiveness, the regulation of its expression is still not fully elucidated and could implicate epigenetic mechanisms. The aim of this study was to analyze the effects of the Histone Deacetylase Inhibitor (HDI) trichostatin A (TSA) and the inhibitor of DNA methylation 5-aza-2'-deoxycytidine (5-azadC) on the proMMP-1 expression in the human HT1080 fibrosarcoma cell line. Real-time RT-PCR revealed that 5-azadC or 5-azadC + TSA but not TSA alone, despite global histone H4 hyperacetylation, increased proMMP-1 mRNA levels. This tran...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659672</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659672</guid>        </item>
        <item>
            <title>Targeting of IL-2 and GM-CSF immunocytokines to a tumor vaccine leads to increased anti-tumor activity.</title>
            <link>http://www.medworm.com/index.php?rid=4659671&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424118%26dopt%3DAbstract</link>
            <description>In this study, we combined such immunocytokines with the tumor vaccine ATV-NDV consisting of irradiated tumor cells infected with Newcastle disease virus (NDV). The two fusion proteins bsF-GMCSF and tsHN-IL2-GM-CSF, binding, respectively, to the viral fusion protein (F) or to hemagglutinin-neuraminidase (HN) expressed on the surface of the vaccine cells and containing GM-CSF or GM-CSF and IL-2-activities were produced by recombinant antibody technology. The purified molecules showed the expected binding specificity and biological activity inherent to the respective cytokine. Using a newly established in vitro tumor neutralisation assay (TNA), we showed improved antitumoral effect through tumor growth inhibition when human peripheral blood mononuclear cells from healthy donors were stimula...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659671</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659671</guid>        </item>
        <item>
            <title>Pancratistatin induces apoptosis and autophagy in metastatic prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4659670&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424119%26dopt%3DAbstract</link>
            <description>This study presents the novel finding that pancratistatin treatment caused decreased migration capacity and increased autophagy levels in metastatic prostate cancer cells. Importantly, in this proof-of-concept study, pancratistatin reduced the volume of xenograft tumors compared to control-treated animals, and was well-tolerated. Our results highlight the potential of pancratistatin for clinical development as a selective therapeutic for treatment of metastatic prostate cancer.
    PMID: 21424119 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659670</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659670</guid>        </item>
        <item>
            <title>Deleterious MnSOD signals lead to abnormal breast cell proliferation by radiation and estrogen exposure.</title>
            <link>http://www.medworm.com/index.php?rid=4659669&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424120%26dopt%3DAbstract</link>
            <description>Authors: Echiburú-Chau C, Roy D, Calaf GM
    Manganese superoxide dismutase (MnSOD) seems to have a pivotal role in mantaining the normal phenotype by suppressing cell growth through blocking the entrance of quiescent cells into the cell cycle. MnSOD protein expression has been shown to be dysregulated in malignant cells. A well-established experimental breast epithelial cell cancer model was used to observe the relationship in the presence or absence of such protein and the phenotype of the cells. This model was derived from the spontaneously immortalized breast epithelial cell line MCF-10F, which was transformed with estrogen and radiation. The results of this study showed that deleterious expression of MnSOD enhanced the malignant phenotype demonstrated by cell cycle protein expressio...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659669</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659669</guid>        </item>
        <item>
            <title>The novel resveratrol analog HS-1793-induced polyploid LNCaP prostate cancer cells are vulnerable to downregulation of Bcl-xL.</title>
            <link>http://www.medworm.com/index.php?rid=4659668&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424121%26dopt%3DAbstract</link>
            <description>We examined the antitumor activity exerted by HS-1793 in prostate cancer cells, and we observed that HS-1793 acts as a polyploidy inducer. Noticeably, multinucleation and polyploidization were induced in most LNCaP cells treated with HS-1793 at the dose causing a slight decline in cell viability. However, the induction of multinucleation and polyploidization was much lower in PC-3 prostate cancer cells treated with the same dose of HS-1793. Western blot and RT-PCR analyses showed that the expression of Aurora B was almost undetectable in LNCaP cells, but it was highly expressed in PC-3 cells. Further, silencing of Aurora B sensitized PC-3 cells to HS-1793-induced multi-nucleation. These results indicate that expression of Aurora B determines multinucleation in prostate cancer cells treated...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659668</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659668</guid>        </item>
        <item>
            <title>Nuclear receptor CAR-regulated expression of the FAM84A gene during the development of mouse liver tumors.</title>
            <link>http://www.medworm.com/index.php?rid=4659667&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21424122%26dopt%3DAbstract</link>
            <description>Authors: Kamino H, Yamazaki Y, Saito K, Takizawa D, Kakizaki S, Moore R, Negishi M
    The nuclear xenobiotic receptor CAR is a phenobarbital (PB)-activated transcription factor. Using a mouse model of two-step liver tumorigenesis, in which tumor growth was initiated by diethyl nitrosamine (DEN) and promoted by chronic treatment with PB, we previously demonstrated that tumors developed only in the presence of CAR. Here, we have identified the FAM84A (family with sequence similarity 84, member A) gene as a CAR-regulated gene that is over-expressed during development of phenobarbital-promoted mouse liver tumors. FAM84A mRNA was induced in the liver of DEN/PB-treated mice prior to the development of liver tumors and this induction continued in the non-tumor as well as tumor tissues of a tumor...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4659667</comments>
            <pubDate>Thu, 17 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4659667</guid>        </item>
        <item>
            <title>Frequent somatic demethylation of RAPGEF1/C3G intronic sequences in gastrointestinal and gynecological cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4600584&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399874%26dopt%3DAbstract</link>
            <description>Authors: Samuelsson J, Alonso S, Ruiz-Larroya T, Cheung TH, Wong YF, Perucho M
    RAPGEF1 (also known as C3G and GRF2) is a guanine nucleotide exchange factor that releases GDP from the inactive Rap1 protein, facilitating its subsequent activation by the binding of GTP. Rap1 plays regulatory roles in proliferation, differentiation and apoptosis. Amplification and overexpression of RAPGEF1 have been found in small cell lung cancers, suggesting an oncogenic role. In contrast, hypermethylation of a promoter CpG island (CGI-A) of RAPGEF1 has been reported in squamous cervical tumors, suggesting an anti-oncogenic role in these gynecological cancers. In our studies of DNA methylation alterations in gastrointestinal cancer we found somatic demethylation of a relaxed-criterion CpG island (CGI-B) ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600584</comments>
            <pubDate>Fri, 11 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600584</guid>        </item>
        <item>
            <title>SV40 and p53 as team players in childhood lymphoproliferative disorders.</title>
            <link>http://www.medworm.com/index.php?rid=4600589&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399869%26dopt%3DAbstract</link>
            <description>We examined 91 lymphomas [60 B-cell non-Hodgkin's lymphomas (B-NHLs), 19 B-cell acute lymphoblastic leukemias (B-ALLs), 7 B-cell precursor acute lymphoblastic leukemias and 5 T-cell acute lymphoblastic leukemias] for the presence of SV40. Overall, 40 samples from 12 B-NHL/19 B-ALL patients were additionally investigated for p53 mutation in the hot-spot exons 5 to 8. Overall, we found 62/91 lymphomas to be SV40-positive, among them 16/19 B-ALLs and 38/60 B-NHLs. SV40 was absent in 147 of the 149 blood control samples. We found 11 p53 mutations in 19 B-ALL patients: 5 in exon 5 (codons 132, 141, 143, 155 and 181), 4 in exon 7 (codons 236, 238 and 248), 2 in exon 8 (codon 273). In B-NHL patients we found p53-mutations in 9/12 samples: 6 of these in 3 lymph nodes (LNs). One LN harboured 3 diff...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600589</comments>
            <pubDate>Thu, 10 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600589</guid>        </item>
        <item>
            <title>Selective enrichment of hypericin in malignant glioma: Pioneering in vivo results.</title>
            <link>http://www.medworm.com/index.php?rid=4600588&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399870%26dopt%3DAbstract</link>
            <description>Authors: Noell S, Mayer D, Strauss WS, Tatagiba MS, Ritz R
    Malignant gliomas are diffuse infiltrative growing tumors with a poor prognosis despite treatment with a combination of surgery, radiotherapy and chemotherapy. It has been shown recently that complete tumor resection improves the survival time significantly. Hypericin, a component of St. Johns Wort, is one of the most powerful photosensitizers in nature. The aim of the present study was to investigate accumulation of hypericin in intracerebral implanted malignant glioma in vivo. Rats underwent stereotactic implantation of C6 glioma cells. After intravenous administration of hypericin (5 mg per kg body weight), accumulation of the compound was studied in tumor, the infiltration zone surrounding the tumor and healthy brain (contr...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600588</comments>
            <pubDate>Thu, 10 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600588</guid>        </item>
        <item>
            <title>MicroRNA miR-125b is a prognostic marker in human colorectal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4600587&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399871%26dopt%3DAbstract</link>
            <description>Authors: Nishida N, Yokobori T, Mimori K, Sudo T, Tanaka F, Shibata K, Ishii H, Doki Y, Kuwano H, Mori M
    MicroRNAs (miRNAs) are small, non-coding RNAs that can function as oncogenes or tumor suppressors in human cancer. Recent reports have highlighted the oncogenic aspects of microRNA miR-125b. However, the clinical significance of miR-125b in gastrointestinal cancers has not been sufficiently investigated. To this end, we analyzed miR-125b expression in colorectal cancer cases. Quantitative RT-PCR was used to evaluate miR-125b expression in 89 colorectal cancer cases to determine the clinicopathological significance of miR-125b expression. The high miR-125b expression group showed a greater incidence of advanced tumor size and tumor invasion compared to the low miR-125b expression gro...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600587</comments>
            <pubDate>Thu, 10 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600587</guid>        </item>
        <item>
            <title>microRNA-34 family and treatment of cancers with mutant or wild-type p53 (Review).</title>
            <link>http://www.medworm.com/index.php?rid=4600586&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399872%26dopt%3DAbstract</link>
            <description>Authors: Wong MY, Yu Y, Walsh WR, Yang JL
    In the last decade, microRNAs (miRNAs; small noncoding RNA molecules) as post-transcriptional regulators have been a hotspot in research for their involvement in biological processes and tumour development. However, there have been few reviews focusing on a single miRNA family. The dysregulation of miRNAs appears to play a crucial role in cancer pathogenesis where they exert their effect as oncogenes or as tumour suppressors. This review summarises current studies on the dysregulation of the microRNA-34 (miR-34) family in different types of cancers and its role in the p53 network. The structure of the miR-34 family members includes p53-binding sites reflecting their function as tumour suppressors downstream of the p53 pathway. miR-34 dysregulat...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600586</comments>
            <pubDate>Thu, 10 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600586</guid>        </item>
        <item>
            <title>Antitumor activity of nifurtimox is enhanced with tetrathiomolybdate in medulloblastoma.</title>
            <link>http://www.medworm.com/index.php?rid=4600585&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399873%26dopt%3DAbstract</link>
            <description>Authors: Koto KS, Lescault P, Brard L, Kim K, Singh RK, Bond J, Illenye S, Slavik MA, Ashikaga T, Saulnier Sholler GL
    Medulloblastoma, a neuroectodermal tumor arising in the cerebellum, is the most common brain tumor found in children. We recently showed that nifurtimox induces production of reactive oxygen species (ROS) and subsequent apoptosis in neuroblastoma cells both in vitro and in vivo. Tetrathiomolybdate (TM) has been shown to decrease cell proliferation by inhibition of superoxide dismutase-1 (SOD1). Since both nifurtimox and TM increase ROS levels in cells, we investigated whether the combination of nifurtimox and TM would act synergistically in medulloblastoma cell lines (D283, DAOY). Genome-wide transcriptional analysis, by hybridizing RNA isolated from nifurtimox and TM a...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600585</comments>
            <pubDate>Thu, 10 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600585</guid>        </item>
        <item>
            <title>p53, HER2 and tumor cell apoptosis correlate with clinical outcome after neoadjuvant bevacizumab plus chemotherapy in breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4600590&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399868%26dopt%3DAbstract</link>
            <description>Authors: Yang SX, Steinberg SM, Nguyen D, Swain SM
    Bevacizumab, an antibody to vascular endothelial growth factor (VEGF), has been incorporated into chemotherapy regimens in the treatment of several cancer types including breast cancer. The aim of this study was to identify tumor and angiogenic factors that potentially associate with outcome. In a pilot trial, 21 patients with inflammatory breast cancer and locally advanced breast cancer received bevacizumab plus doxorubicin-docetaxel chemotherapy before surgery. Baseline p53, HER2, tumor apoptosis, Ki67, estrogen receptor (ER), VEGF-A, serum VEGF (sVEGF), VEGFR2-Y951 and microvessel density (MVD) were prospectively designed and determined by immunohistochemistry and enzyme-linked immunosorbent assay. Hazard ratios (HR) and 95% confide...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600590</comments>
            <pubDate>Wed, 09 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600590</guid>        </item>
        <item>
            <title>Temozolomide-induced modification of the CXC chemokine network in experimental gliomas.</title>
            <link>http://www.medworm.com/index.php?rid=4600592&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399866%26dopt%3DAbstract</link>
            <description>In conclusion, TMZ affects the expression and secretion of CXCL2 (and, to a lesser extent, CXCL3 and CXCL8) in glioma cells, and CXCL2 directly impacts glioma cell biology.
    PMID: 21399866 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600592</comments>
            <pubDate>Tue, 08 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600592</guid>        </item>
        <item>
            <title>Ganoderma lucidum exerts anti-tumor effects on ovarian cancer cells and enhances their sensitivity to cisplatin.</title>
            <link>http://www.medworm.com/index.php?rid=4600591&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21399867%26dopt%3DAbstract</link>
            <description>In this study, we determined whether Ganoderma lucidum regulates EOC cell activity. Using several cell lines derived from EOC, we found that Ganoderma lucidum strongly decreased cell numbers in a dose-dependent manner. Ganoderma lucidum also inhibited colony formation, cell migration and spheroid formation. In particular, Ganoderma lucidum was effective in inhibiting cell growth in both chemosensitive and chemoresistant cells and the treatment with Ganoderma lucidum significantly enhanced the effect of cisplatin on EOC cells. Furthermore, Ganoderma lucidum induced cell cycle arrest at the G2/M phase and also induced apoptosis by activating caspase 3. Finally, Ganoderma lucidum increased p53 but inhibited Akt expression. Taken together, these findings suggest that Ganoderma lucidum exerts m...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600591</comments>
            <pubDate>Tue, 08 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600591</guid>        </item>
        <item>
            <title>Regulation of cancer cell proliferation by caveolin-2 down-regulation and re-expression.</title>
            <link>http://www.medworm.com/index.php?rid=4600600&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373752%26dopt%3DAbstract</link>
            <description>Authors: Lee S, Kwon H, Jeong K, Pak Y
    We investigated whether altering caveolin-2 (cav-2) expression affects the proliferation of cancer cells. Cav-2 was not detected in HepG2, SH-SY5Y and LN-CaP cells, and the loss of cav-2 expression was not restored by 5-aza-2'-deoxycytidine treatment. In contrast, C6, HeLa, A549, MCF7 and PC3M cells expressed cav-2. Effects of re-expression of exogenous cav-2 in HepG2, SH-SY5Y and LN-CaP cells, and siRNA-mediated down-regulation of endogenous cav-2 in C6, HeLa, A549, MCF7 and PC3M cells on cancer proliferation were examined by MTT assay, colony formation assay and flow cytometric analysis. Cav-2 transfection in HepG2 hepatocellular carcinoma cells and knockdown in C6 glioma cells caused reduction in cell proliferation and growth with retarded entr...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600600</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600600</guid>        </item>
        <item>
            <title>Alteration of p53-binding protein 1 expression as a risk factor for local recurrence in patients undergoing resection for extrahepatic cholangiocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4600599&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373753%26dopt%3DAbstract</link>
            <description>In conclusion, after resection for extrahepatic cholangiocarcinoma, clinically evident local recurrence at ductal stumps is closely associated with 53BP1 inactivation and decreased apoptosis.
    PMID: 21373753 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600599</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600599</guid>        </item>
        <item>
            <title>Combined GM-CSF treatment and M-CSF inhibition of tumor-associated macrophages induces dendritic cell-like signaling in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=4600596&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373754%26dopt%3DAbstract</link>
            <description>Authors: Kitoh Y, Saio M, Gotoh N, Umemura N, Nonaka K, Bai J, Vizkeleti L, Torocsik D, Balazs M, Adany R, Takami T
    Macrophages demonstrate plasticity, and tumor-associated macrophages (TAM) can function as immunosuppressive cells in the tumor microenvironment. Therefore, in this study, we aimed to reprogram TAM in vitro with cytokine signal alteration. Granulocyte macrophage colony stimulating factor (GM-CSF) treatment alone did not lead to changes in the expression of M1 (including IL-1β, TNFα and CXCL-10) or M2 (including CD36, CD206 and CCL17) molecules by TAM in vitro, although they adopted a round morphology and were less adhesive to the culture dish. When macrophage colony stimulating factor (M-CSF) signals were suppressed by siRNA against the M-CSF receptor (M-CSFR) in conju...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600596</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600596</guid>        </item>
        <item>
            <title>Microarray-based analysis: Identification of hypoxia-regulated microRNAs in retinoblastoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4600595&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373755%26dopt%3DAbstract</link>
            <description>In this study, we aimed to analyze the pattern of miRNA expression in a retinoblastoma cell line under hypoxic conditions and to identify the miRNAs regulated by hypoxia, as well as their possible functions. miRNA expression profiling in retinoblastoma cells (HXO-RB44) under normal and hypoxic conditions was assessed by microarray techniques. The differentially expressed miRNAs were subjected to bioinformatic analyses to predict and categorise the key miRNAs and their target genes. A quantitative real-time RT-PCR approach was used to validate their expression. A Cell Counting kit was used to evaluate the functional significance of miR-181b in RB cell proliferation. There were 46 miRNAs that changed expression more than 2-fold in response to hypoxia (34 up-regulated and 12 down-regulated). ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600595</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600595</guid>        </item>
        <item>
            <title>Potent anti-tumor killing activity of the multifunctional Treg cell line HOZOT against human tumors with diverse origins.</title>
            <link>http://www.medworm.com/index.php?rid=4600594&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373756%26dopt%3DAbstract</link>
            <description>Authors: Inoue T, Tashiro Y, Takeuchi M, Otani T, Tsuji-Takayama K, Okochi A, Mukae Y, Koreishi M, Yamasaki F, Kumon H, Nakamura S, Kibata M, Kondo E
    The T cell line HOZOT has a unique FOXP3+CD4+ CD8+CD25+ phenotype, exhibits suppressive activity in allogeneic mixed lymphocyte reactions (MLR), and produces IL-10, defining HOZOT as regulatory T cells (Tregs). Interestingly, in addition to possessing a suppressive Treg ability, HOZOT was also found to show cytotoxicity against certain representative human cancer cell types. In order to disclose the range of anti-tumor activity by HOZOT, we screened it by using a panel of twenty human tumor cell lines with different origins. Consequently, HOZOT showed potent cytocidal effects against a wide spectrum of neoplastic cells including carcinoma...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600594</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600594</guid>        </item>
        <item>
            <title>Auto-stimulatory action of secreted caveolin-1 on the proliferation of Ewing's sarcoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4600593&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21373757%26dopt%3DAbstract</link>
            <description>Authors: Sengupta A, Mateo-Lozano S, Tirado OM, Notario V
    Caveolin-1 (CAV1) is highly expressed in Ewing's sarcoma (EWS). We previously showed that increased cellular CAV1 is associated with the regulation of the tumorigenicity, drug resistance and metastatic ability of EWS cells. Because several studies reported that melanoma and prostate cancer cells, which express relatively high CAV1 levels, secrete CAV1, and that secreted CAV1 is associated with tumor progression, our study explored the possibility that EWS cells also secreted CAV1 and that secreted CAV1 may contribute to EWS pathobiology. Results from experiments involving the ectopic expression of a Myc-tagged CAV1 protein in EWS cells as well as the supplementation of culture media with purified CAV1 protein followed by its int...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600593</comments>
            <pubDate>Thu, 03 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600593</guid>        </item>
        <item>
            <title>Lithium reduces tumorigenic potential in response to EGF signaling in human colorectal cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4600604&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369697%26dopt%3DAbstract</link>
            <description>In this study, we investigated whether the Wnt/β-catenin and EGFR pathways converge to modulate the malignant potential of CRC. We used Caco-2 cells, a well-established model used to study CRC, and treatments with lithium chloride, as a modulator of the Wnt/β-catenin pathway, and with EGF as an inducer of EGFR signaling. We found that both agents altered the subcellular distribution of claudin-1 and β-catenin, two important proteins of the apical junctional complex, but not their abundance in the cell. Nuclear stabilization of β-catenin, a marker of Wnt pathway activation, was observed after treatment with both compounds. However, lithium, but not EGF, inhibited GSK3-β, indicating that these agents modulate this enzyme in a differential fashion. Furthermore, EGF treatment increased th...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600604</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600604</guid>        </item>
        <item>
            <title>PLU-1/JARID1B/KDM5B is required for embryonic survival and contributes to cell proliferation in the mammary gland and in ER+ breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4600603&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369698%26dopt%3DAbstract</link>
            <description>Authors: Catchpole S, Spencer-Dene B, Hall D, Santangelo S, Rosewell I, Guenatri M, Beatson R, Scibetta AG, Burchell JM, Taylor-Papadimitriou J
    The four members of the JARID1/KDM5 family of proteins, a sub-group of the larger ARID (AT rich DNA binding domain) family, have been shown to demethylate trimethylated lysine 4 on histone 3 (H3K4me3), a chromatin mark associated with actively transcribed genes. In some lower organisms a single homologue of JARID1 is found, and functions of the four proteins found in mice and humans may be specific or overlapping. To investigate the function of the Jarid1B protein we examined the effects of deletion of the gene in mice. Systemic knock out of Jarid1b resulted in early embryonic lethality, whereas mice not expressing the related Jarid1A gene are ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600603</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600603</guid>        </item>
        <item>
            <title>Antitumor activity of a novel small molecule STAT3 inhibitor against a human lymphoma cell line with high STAT3 activation.</title>
            <link>http://www.medworm.com/index.php?rid=4600601&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21369699%26dopt%3DAbstract</link>
            <description>Authors: Ashizawa T, Miyata H, Ishii H, Oshita C, Matsuno K, Masuda Y, Furuya T, Okawara T, Otsuka M, Ogo N, Asai A, Akiyama Y
    Signal transducer and activator of transcription (STAT)3, a member of a family of DNA-binding molecules mediating numerous physiological and oncogenic signaling pathways, is a novel target in cancer cells which show high phosphorylation of STAT3. Recently, we identified a novel small-molecule inhibitor of STAT3 dimerization, STX-0119, as a cancer therapeutic. We investigated the mechanisms responsible for the antitumor activity in vitro and in vivo through numerous biochemical and biological assays. Specifically, the effects of STX-0119 on target genes (c-myc, cyclin D1, survivin) and apoptosis induction were analyzed in tumors treated with STX-0119 in vivo. ST...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600601</comments>
            <pubDate>Mon, 28 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600601</guid>        </item>
        <item>
            <title>CCL25 mediates migration, invasion and matrix metalloproteinase expression by breast cancer cells in a CCR9-dependent fashion.</title>
            <link>http://www.medworm.com/index.php?rid=4537519&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21344163%26dopt%3DAbstract</link>
            <description>Authors: Johnson-Holiday C, Singh R, Johnson E, Singh S, Stockard CR, Grizzle WE, Lillard JW
    Breast cancer (BrCa) is one of the most frequently diagnosed cancers and the second leading cause of cancer-related deaths in North American women. Most deaths are caused by metastasis, and BrCa is characterized by a distinct metastatic pattern involving lymph nodes, bone marrow, lung, liver and brain. Migration of metastatic cells share many similarities with leukocyte trafficking, which are regulated by chemokines and their receptors. The current study evaluates the expression and functional role of CCR9, and its only known ligand, CCL25, in BrCa cell migration and invasion. Quantitative immunohistochemical analysis showed that both moderately and poorly differentiated BrCa tissue expressed s...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537519</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4537519</guid>        </item>
        <item>
            <title>Synergistic antitumor effect of interferon-ß with gemcitabine in interferon-α-non-responsive pancreatic cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4537518&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21347515%26dopt%3DAbstract</link>
            <description>In conclusion, our results indicated that the growth-inhibitory effect of IFN-ß with gemcitabine was synergistic not only in pancreatic cancer cells with strong expression of IFNAR2, but also in those with weak expression of IFNAR2.
    PMID: 21347515 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537518</comments>
            <pubDate>Wed, 23 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4537518</guid>        </item>
        <item>
            <title>Expression of B7-H3 in hypopharyngeal squamous cell carcinoma as a predictive indicator for tumor metastasis and prognosis.</title>
            <link>http://www.medworm.com/index.php?rid=4537523&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21344157%26dopt%3DAbstract</link>
            <description>Authors: Katayama A, Takahara M, Kishibe K, Nagato T, Kunibe I, Katada A, Hayashi T, Harabuchi Y
    B7-H3 is a member of the B7 family thought to be a co-regulatory factor of antigen-specific T-cell immune response via co-stimulatory and co-inhibitory receptors. We evaluated its potential expression in head and squamous cell carcinoma (SCC) cell lines, and in clinical tissue samples obtained from 37 patients with human hypopharyngeal SCC. All head and neck SCC cell lines tested expressed both the B7-H3 gene and cell surface protein. The staining intensity of immunoreactivity by tumor cells was blindly evaluated by two head and neck surgeons and the results were categorized into 4 grades according to staining intensity. Eighty-seven percent of patients expressed B7-H3. B7-H3 expression was...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537523</comments>
            <pubDate>Tue, 22 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4537523</guid>        </item>
        <item>
            <title>Effect of PP2A on p34SEI-1 expression in response to ionizing radiation in MCF-7 human breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4537522&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21344158%26dopt%3DAbstract</link>
            <description>Authors: Jung S, Jeong HK, Shin J, Lee MS
    Breast cancer is one of the most common cancers in women and it is highly treatable by radiotherapy and/or radiochemotherapy. A global analysis of the protein expression pattern was performed to identify radiation-responsive proteins in MCF-7 breast cancer cells using 2D-PAGE coupled with MALDI-TOF-MS. When MCF-7 cells were exposed to ionizing radiation (IR) such as γ-rays, eight proteins (GH2, RGS17, BAK1, CCNH, TSG6, RAD51B, IGFBP1, and CASP14) were up-regulated and three proteins (C1QRF, PLSCR2, and p34SE1-1) were down-regulated. In an effort to find what mechanisms are responsible for these changes, we initially focused on p34SE1-1, which is known as a transcriptional regulator and oncogene. Our results show that p34SE1-1 expression is sig...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537522</comments>
            <pubDate>Tue, 22 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4537522</guid>        </item>
        <item>
            <title>(-)-Epigallocatechin-3-gallate induces apoptosis in gastric cancer cell lines by down-regulating survivin expression.</title>
            <link>http://www.medworm.com/index.php?rid=4537521&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21344159%26dopt%3DAbstract</link>
            <description>This study provides a novel mechanism whereby EGCG potentially inhibits cancer cell growth, concluding that EGCG may be a potential candidate in anti-survivin cancer therapy.
    PMID: 21344159 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537521</comments>
            <pubDate>Tue, 22 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4537521</guid>        </item>
        <item>
            <title>The novel synthesized 2-(3-(methylamino)phenyl)-6-(pyrrolidin-1-yl)quinolin-4-one (Smh-3) compound induces G2/M phase arrest and mitochondrial-dependent apoptotic cell death through inhibition of CDK1 and AKT activity in HL-60 human leukemia cells.</title>
            <link>http://www.medworm.com/index.php?rid=4537520&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21344160%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effects of 2-(3-(methylamino)phenyl)-6-(pyrrolidin-1-yl)quinolin-4-one (Smh-3) on viability, cell cycle and apoptotic cell death which occurred in different leukemia cell lines (HL-60, U937 and K562) in a dose- and time-dependent manner, but which did not obviously impair the viability of normal human umbilical vein endothelial cells (HUVEC) in vitro. The approximate IC50 was 103.26±4.59 nM for a 48 h treatment in HL-60 cells. Cell cycle analysis showed that 100 nM Smh-3 induced signi-ficant G2/M arrest in examined cells. Within 0, 12, 24 and 48 h of treatment, Smh-3 inhibited CDK1 activity and decreased protein levels of CDK1, cyclin A and cyclin B. Smh-3-induced chromatin condensation and DNA fragmentation were determined by DAPI and TUNEL staining. C...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537520</comments>
            <pubDate>Tue, 22 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4537520</guid>        </item>
        <item>
            <title>Roles of cyclin-dependent kinase 8 and β-catenin in the oncogenesis and progression of gastric adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4537525&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21344156%26dopt%3DAbstract</link>
            <description>Authors: Kim MY, Han SI, Lim SC
    Gastric adenocarcinoma is a common cause of cancer-related death. The Wnt/β-catenin pathway plays an important role in various cancers. However, relatively little is known about the regulatory mechanism of β-catenin in stomach cancer. To determine the patterns of cyclin-dependent kinase (CDK) 8 and β-catenin expression and the relationship between CDK8 and β-catenin, we conducted a study of immuno-histochemical staining of tumor tissues (12 adenomas, 24 early gastric carcinomas, 24 advanced gastric carcinomas and 21 metastatic lymph nodes), together with Western blot analysis and CDK8 interference studies using gastric cancer cell lines. Gastric adenocarcinomas with CDK8 expression had distinct clinical, prognostic and molecular attributes. CDK8 expr...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537525</comments>
            <pubDate>Fri, 18 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4537525</guid>        </item>
        <item>
            <title>Morphological and cytoskeletal alterations of nervous system tumor cells with different culturing methods.</title>
            <link>http://www.medworm.com/index.php?rid=4537528&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21331444%26dopt%3DAbstract</link>
            <description>In conclusion, this study demonstrated that nervous system tumor cells showed different alterations in morphology, and different cytoskeletal protein expression patterns, depending on the culture methods.
    PMID: 21331444 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537528</comments>
            <pubDate>Thu, 17 Feb 2011 00:00:00 +0100</pubDate>
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            <title>Detection of prostate-specific membrane antigen on HUVECs in response to breast tumor-conditioned medium.</title>
            <link>http://www.medworm.com/index.php?rid=4537527&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21331445%26dopt%3DAbstract</link>
            <description>Authors: Liu T, Jabbes M, Nedrow-Byers JR, Wu LY, Bryan JN, Berkman CE
    Prostate-specific membrane antigen (PSMA), a well-known biomarker of prostate cancer, has also been found to be highly expressed in the neovasculature of multiple non-prostatic solid tumors. As a consequence, it has the potential to become a biomarker for tumor-associated vasculature. Herein, we describe an in vitro model for assessing PSMA expression associated with tube formation by primary human umbilical vein endothelial cells (HUVECs) cultured in Matrigel and induced by tumor-conditioned medium (TCM) derived from human breast cancer cells (MDA-MB-231). In contrast to vascular endothelial growth factor (VEGF)-containing endothelial cell medium, TCM induced higher expression of PSMA in HUVECs. The vessel-like tub...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537527</comments>
            <pubDate>Thu, 17 Feb 2011 00:00:00 +0100</pubDate>
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            <title>Pooled analysis of case-control studies on malignant brain tumours and the use of mobile and cordless phones including living and deceased subjects.</title>
            <link>http://www.medworm.com/index.php?rid=4537526&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21331446%26dopt%3DAbstract</link>
            <description>In conclusion, an increased risk was found for glioma and use of mobile or cordless phone. The risk increased with latency time and cumulative use in hours and was highest in subjects with first use before the age of 20.
    PMID: 21331446 [PubMed - as supplied by publisher] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4537526</comments>
            <pubDate>Thu, 17 Feb 2011 00:00:00 +0100</pubDate>
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            <title>Genetic variants at the miR-124 binding site on the cytoskeleton-organizing IQGAP1 gene confer differential predisposition to breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4483278&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21318219%26dopt%3DAbstract</link>
            <description>Authors: Zheng H, Song F, Zhang L, Yang D, Ji P, Wang Y, Almeida M, Calin GA, Hao X, Wei Q, Zhang W, Chen K
    IQGAP1 knockout mice develop gastric cancer, but the IQGAP1 protein is associated with some advanced-stage human cancers. IQGAP1 expression is regulated by a microRNA, miR-124, through a binding site at the 3'-untranslated region, where a single nucleotide polymorphism (SNP) exists in the core binding region. We asked whether IQGAP1 expression is associated with breast cancer development and whether genetic variants at the miR-124 binding site are important. We genotyped the IQGAP1 SNP rs1042538 A/T in 1,541 breast cancer cases and 1,598 controls and analyzed the frequency of the variant and interactions with major risk factors in these populations. We also measured the expressio...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4483278</comments>
            <pubDate>Fri, 11 Feb 2011 00:00:00 +0100</pubDate>
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            <title>In vitro transformation of MCF-10A cells by sera harvested from heifers two months post-Zeranol implantation.</title>
            <link>http://www.medworm.com/index.php?rid=4483277&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21318220%26dopt%3DAbstract</link>
            <description>Authors: Ye W, Xu P, Zhong S, Jen R, Threlfall WR, Frasure CV, Feng E, Li H, Lin SH, Liu JY, Lin YC
    Among many risk factors of breast cancer, estrogens and non-estrogenic endocrine disruptors are considered to play critical roles in human breast carcinogenesis. Zeranol (Z) is a non-steroidal agent with potent estrogenic activity and has been widely used as an FDA approved beef growth promoter in the US. Recently, concerns have been raised about the potential adverse health risk by consumption of products containing biologically active Z and its metabolites. By utilizing cell proliferation assay, soft agar assay, quantitative real-time PCR and Western blotting analysis, we examined the potentially tumorigenic activity of bio-active Z containing sera harvested from heifers two months pos...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4483277</comments>
            <pubDate>Fri, 11 Feb 2011 00:00:00 +0100</pubDate>
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            <title>Signalling pathways involved in endocrine resistance in breast cancer and associations with epithelial to mesenchymal transition (Review).</title>
            <link>http://www.medworm.com/index.php?rid=4483276&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21318221%26dopt%3DAbstract</link>
            <description>Authors: Al Saleh S, Sharaf LH, Luqmani YA
    Both de novo and acquired endocrine resistance constitute a major therapeutic problem for treatment of hormone-positive breast cancer. Multiple explanatory mechanisms have been proposed through the study of cellular models which focus principally on receptor tyrosine kinase mediated signalling pathways utilizing src, PI3K, MAPK and Smads. Many of the transducing molecules, particularly nuclear transcription factors such as Snail, Twist, Snail2, ZEB, FOXC2, TCF/LEF and Goosecoid are participants in proliferation as well as invasion and metastasis, involving a process of orchestrated cellular remodeling which is being likened to the process of epithelial to mesenchymal transition that takes place during embryonic development. We review the accum...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4483276</comments>
            <pubDate>Fri, 11 Feb 2011 00:00:00 +0100</pubDate>
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            <title>Histone deacetylase inhibition modulates deoxyribonucleotide pools and enhances the antitumor effects of the ribonucleotide reductase inhibitor 3'-C-methyladenosine in leukaemia cells.</title>
            <link>http://www.medworm.com/index.php?rid=4483275&amp;cid=s_36721_6_f&amp;fid=36721&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21318222%26dopt%3DAbstract</link>
            <description>Authors: Meli M, Tolomeo M, Grifantini M, Mai A, Cappellacci L, Petrelli R, Rotili D, Ferro A, Saiko P, Szekeres T, Dusonchet L
    Histone deacetylase (HDAC) inhibitors are a new class of epigenetic agents that were reported to enhance the cytotoxic effects of classical anticancer drugs through multiple mechanisms. However, which of the possible drug combinations would be the most effective and clinically useful are to be determined. We treated the HL60 and NB4 promyelocytic leukaemia cells with a combination of the ribonucleotide reductase (RR) inhibitor 3'-C-methyladenosine (3'-Me-Ado) and several hydroxamic acid-derived HDAC inhibitors, including two recently synthesized molecules, MC1864 and MC1879, and the reference compound trichostatin A (TSA). The results showed significant growth...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
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            <pubDate>Fri, 11 Feb 2011 00:00:00 +0100</pubDate>
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