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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>Sat, 20 Mar 2010 13:50:31 +0100</lastBuildDate>
        <item>
            <title>Quantification of internalization of EGFR-binding Affibody molecules: Methodological aspects.</title>
            <link>http://www.medworm.com/index.php?rid=3331842&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%3D20198317%26dopt%3DAbstract</link>
            <description>Authors: G&amp;#xF6;string L, Chew MT, Orlova A, H&amp;#xF6;id&amp;#xE9;n-Guthenberg I, Wennborg A, Carlsson J, Frejd FY
    Tumor cell internalization of targeting agents is of interest, since internalization influences the local retention time of a radionuclide and thereby imaging quality in PET and SPECT and effects of radionuclide therapy. In cases where nuclear methods are not applicable at the cellular level, quantitative fluorescent techniques are useful as described in this article. Two fluorescence-based methods to study cellular internalization were applied: the CypHer and the Alexa488-quenching methods, both utilized in fluorescence microscopy and flow cytometry. Two EGFR-binding Affibody molecules were analyzed in A431 cells: the monomer Z1907 and the dimer (Z1907)2. EGF, cetuximab and non...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331842</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:53 +0100</pubDate>
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            <title>MUC2 gene promoter methylation in mucinous and non-mucinous colorectal cancer tissues.</title>
            <link>http://www.medworm.com/index.php?rid=3331841&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%3D20198318%26dopt%3DAbstract</link>
            <description>Authors: Okudaira K, Kakar S, Cun L, Choi E, Wu Decamillis R, Miura S, Sleisenger MH, Kim YS, Deng G
    Abundant mucin production and MUC2 expression is the key feature of mucinous colorectal cancer (CRC). Although MUC2 gene methylation has been thought to play an important role in loss of MUC2 expression, the tissues are difficult to analyze because of the cellular heterogeneity of tissue samples. In the present study, we determined the role of region-specific methylation in the MUC2 promoter in MUC2 expression in CRC. Additionally, we optimized the conditions for quantification of methylation analysis in mucinous and non-mucinous CRC tissues. We identified two regions in MUC2 promoter, region A (-289 and -274) and region C (-193 and -160), that correlated with loss of MUC2 expression by...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331841</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:50 +0100</pubDate>
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        <item>
            <title>Targeted photodynamic therapy for prostate cancer: Inducing apoptosis via activation of the caspase-8/-3 cascade pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3331840&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%3D20198319%26dopt%3DAbstract</link>
            <description>Authors: Liu T, Wu LY, Choi JK, Berkman CE
    The limitation of specific delivery of photosensitizers to tumor sites, represents a significant shortcoming of photodynamic therapy (PDT) application at present. Prostate-specific membrane antigen (PSMA), a validated biomarker for prostate cancer, has attracted considerable attention as a target for imaging and therapeutic applications for prostate cancer. The present study focuses on the investigation of a PSMA inhibitor-conjugate of pyropheophorbide-a (Ppa-conjugate 2.1) for a targeted PDT application and the mechanism of its mediated-cell death in prostate cancer cells. Multiple fluorescence labeling methods were employed to monitor PDT-treated prostate cancer cells by confocal laser scanning microscopy. Our results demonstrate that Ppa-co...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331840</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:47 +0100</pubDate>
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            <title>HIF1-positive and HIF1-negative glioblastoma cells compete in vitro but cooperate in tumor growth in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3331839&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%3D20198320%26dopt%3DAbstract</link>
            <description>Authors: Fiorenzo P, Mongiardi MP, Dimitri D, Cozzolino M, Ferri A, Montano N, Trevisi G, Maira G, Battistini L, Falchetti ML, Levi A, Pallini R
    Glioblastoma multiforme (GBM) is characterized by extensive angiogenesis that is mostly orchestrated by the hypoxia inducible factor HIF-1. Deregulation of HIF-1 is believed to contribute to cancer initiation and progression. However, instances have been described in which loss of HIF-1 leads to more aggressive tumors. Here we investigated the consequences of downregulating HIF-1 function in the human GBM cell line TB10, both on cell proliferation in vitro and on tumor growth in vivo. RNA interference targeting the O2-regulated HIF-1alpha subunit efficiently reduced HIF-1alpha expression and transcriptional induction of HIF-1-responsive genes ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331839</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:44 +0100</pubDate>
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        <item>
            <title>Tumor-derived trypsin enhances proliferation of intrahepatic cholangiocarcinoma cells by activating protease-activated receptor-2.</title>
            <link>http://www.medworm.com/index.php?rid=3331838&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%3D20198321%26dopt%3DAbstract</link>
            <description>Authors: Nakanuma S, Tajima H, Okamoto K, Hayashi H, Nakagawara H, Onishi I, Takamura H, Kitagawa H, Fushida S, Tani T, Fujimura T, Kayahara M, Ohta T, Wakayama T, Iseki S, Harada S
    In primary malignant liver tumors, trypsinogen-immunoreactivity was present in 70% of intrahepatic cholangiocarcinoma (ICC) specimens, but absent in hepatocellular carcinoma (HCC) specimens. We suggest the secretion of trypsinogen to be a key difference in biological behavior between ICC and HCC cells. The purpose of this study was to investigate the secretion of tumor-derived trypsin and the expression of its specific receptor, protease-activated receptor-2 (PAR-2), in ICC using cell lines and surgical specimens. The expression of trypsinogen-1 mRNA was observed in three of four ICC cell lines, but none of...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331838</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:41 +0100</pubDate>
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        <item>
            <title>Photoactivation of 9-hydroxypheophorbide alpha triggers apoptosis through the reactive oxygen species-mediated mitochondrial pathway and endoplasmic reticulum stress in AMC-HN-3 laryngeal cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3331837&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%3D20198322%26dopt%3DAbstract</link>
            <description>Authors: He P, Ahn JC, Shin JI, Chung PS
    Photodynamic therapy (PDT) is a promising treatment modality for a variety of cancers. It utilizes light-absorbing compounds combined with direct illumination to generate reactive oxygen species in photosensitizer-targeted tumor cells resulting in the final photodamage of tumors. Recently, we demonstrated that a combination modality of 9-hydroxypheophorbide alpha (9-HPbD)-based PDT and carboplatin exerts enhanced cytotoxic and apoptotic effects on AMC-HN-3 laryngeal cancer cells. The present study aimed to investigate the potential apoptotic pathways initiated by 9-HPbD-PDT-mediated reactive oxygen species (ROS) in AMC-HN-3 cells. Cytotoxicity and apoptosis induced by 9-HPbD-PDT were exhibited in a ROS-dependent manner. Mitochondria and the endo...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331837</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:38 +0100</pubDate>
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        <item>
            <title>Radiation-inducible silencing of uPA and uPAR in vitro and in vivo in meningioma.</title>
            <link>http://www.medworm.com/index.php?rid=3331836&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%3D20198323%26dopt%3DAbstract</link>
            <description>Authors: Rao Gogineni V, Kumar Nalla A, Gupta R, Gorantla B, Gujrati M, Dinh DH, Rao JS
    Stereospecific radiation treatment offers a distinct opportunity for temporal and spatial regulation of gene expression at tumor sites by means of inducible promoters. To this end, a plasmid, pCArG-U2, was constructed by incorporating nine CArG elements (in tandem) of EGR1 gene upstream to uPA and uPAR siRNA oligonucleotides in a pCi-neo vector. Radiation-induced siRNA expression was detected in a meningioma cell line (IOMM-Lee). Immunoblotting and RT-PCR analyses confirmed downregulation of uPA and uPAR. A similar effect was observed in transfected cells followed by H2O2 treatment. Moreover, pre-treatment of transfected cells with N-acetyl L-cysteine blocked the silencing of uPA and uPAR, which fur...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331836</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:35 +0100</pubDate>
            <guid isPermaLink="false">3331836</guid>        </item>
        <item>
            <title>Upregulation of Notch pathway molecules in oral squamous cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3331835&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%3D20198324%26dopt%3DAbstract</link>
            <description>Authors: Hijioka H, Setoguchi T, Miyawaki A, Gao H, Ishida T, Komiya S, Nakamura N
    The constitutive activation of the Notch pathway has been demonstrated in various types of malignancies. However, it remains unclear how the Notch pathway is involved in the pathogenesis of oral squamous cell carcinoma (OSCC). We investigated the expression of Notch pathway molecules in OSCC cell lines and biopsy specimens and examined the effect of Notch pathway inhibition. Reverse transcription-polymerase chain reaction revealed upregulation of Notch1, Notch2, Jagged1, HES1 and HEY1 in both OSCC cell lines and biopsy specimens. Immunohistochemical examination showed that the Notch intracellular domain accumulates in the nucleus of cells in OSCC cell lines and biopsy specimens. In addition, Jagged1 is e...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331835</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:32 +0100</pubDate>
            <guid isPermaLink="false">3331835</guid>        </item>
        <item>
            <title>Downregulation of SS18-SSX1 expression in synovial sarcoma by small interfering RNA enhances the focal adhesion pathway and inhibits anchorage-independent growth in vitro and tumor growth in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=3331834&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%3D20198325%26dopt%3DAbstract</link>
            <description>Authors: Takenaka S, Naka N, Araki N, Hashimoto N, Ueda T, Yoshioka K, Yoshikawa H, Itoh K
    Synovial sarcoma (SS) is an aggressive soft-tissue malignancy characterized by a unique t(X;18) translocation resulting in expression of SS18-SSX fusion protein. In order to investigate the biological function of this fusion protein and to develop a novel therapeutic option, we examined downregulation of SS18-SSX1 expression by small interfering RNA targeting SS18-SSX1 in three human SS cell lines. Microarray analysis comparing SS18-SSX1-silenced cells with control cells in three SS cell lines showed that SS18-SSX1 mainly affected the focal adhesion pathway. In accord with the array data, silencing of SS18-SSX1 enhances adhesion to the extracellular matrix through the induction of expression of m...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331834</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:29 +0100</pubDate>
            <guid isPermaLink="false">3331834</guid>        </item>
        <item>
            <title>Neoplastic progression of the human breast cancer cell line G3S1 is associated with elevation of cytoskeletal dynamics and upregulation of MT1-MMP.</title>
            <link>http://www.medworm.com/index.php?rid=3331833&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%3D20198326%26dopt%3DAbstract</link>
            <description>Authors: Tolde O, R&amp;#xF6;sel D, Mierke CT, Pankov&amp;#xE1; D, Folk P, Vesely P, Br&amp;#xE1;bek J
    The newly established breast cancer cell line G3S1, derived from EM-G3 breast cancer progenitors, was analyzed for functional changes related to neoplastic progression manifested by elevated invasiveness and enhanced capability to degrade gelatin. Degradation of gelatin and invasiveness of G3S1 cells was found to be dependent on the activity of matrix proteinases and actin cytoskeletal dynamics. Therefore, the expression and activity of these proteases was compared in G3S1 and EM-G3 cells. Despite enhanced capability of G3S1 cells to degrade gelatin, these cells exhibited lower levels of secreted extracellular matrix degrading proteases than parental EM-G3 cells. However, the expression of membra...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331833</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:27 +0100</pubDate>
            <guid isPermaLink="false">3331833</guid>        </item>
        <item>
            <title>Regulatory T cell depletion enhances tumor specific CD8 T-cell responses, elicited by tumor antigen NY-ESO-1b in hepatocellular carcinoma patients, in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3331832&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%3D20198327%26dopt%3DAbstract</link>
            <description>In conclusion, the increase in frequency of Treg cells might play a role in suppression of the immune response against HCC and for the design of immunotherapy the incorporation of the Treg cell depletion strategy will achieve potent anti-tumor immunity with therapeutic impact.
    PMID: 20198327 [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=3331832</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:24 +0100</pubDate>
            <guid isPermaLink="false">3331832</guid>        </item>
        <item>
            <title>Development of an oral cancer recurrence mouse model after surgical resection.</title>
            <link>http://www.medworm.com/index.php?rid=3331831&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%3D20198328%26dopt%3DAbstract</link>
            <description>Authors: Behren A, Kamenisch Y, Muehlen S, Flechtenmacher C, Haberkorn U, Hilber H, Myers JN, Bergmann Z, Plinkert PK, Simon C
    Oral squamous cell carcinomas (OSCC) are frequent epithelial malignancies and afflicted with a poor prognosis. The majority of these cancers are treated with surgical resection and local recurrences are predominantly responsible for a fatal outcome. In order to provide a better understanding of the development of these local recurrences after surgical ablation, we developed an orthotopic floor-of-mouth squamous cell carcinoma murine model, in which local recurrences occur at a high frequency (55%, 8 out of 15 mice) within 6-21 days after microsurgical removal of the primary. Expression of the enhanced green fluorescent protein (eGFP) in the cancer cells allows ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331831</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:21 +0100</pubDate>
            <guid isPermaLink="false">3331831</guid>        </item>
        <item>
            <title>Carvedilol in glioma treatment alone and with imatinib in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3331830&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%3D20198329%26dopt%3DAbstract</link>
            <description>Authors: Erguven M, Yazihan N, Aktas E, Sabanci A, Li CJ, Oktem G, Bilir A
    The purpose of the study was to investigate whether carvedilol has an antiproliferative effect alone and whether carvedilol provides an additive, synergistic or antagonistic effect on imatinib mesylate-induced cytotoxicity in both C6 glioma monolayer and spheroid culture. The C6 rat glioma chemoresistant experimental brain tumour cell line, that is notoriously difficult to treat with combination chemotherapy, was used both in monolayer and spheroid cultures. We treated C6 glioma cells with carvedilol alone and a combination of carvedilol and imatinib mesylate at a concentration of 10 microM. Following treatment, we evaluated cell proliferation index, bromodeoxyuridine labelling index (BrDU-LI), cell cycle distri...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331830</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:18 +0100</pubDate>
            <guid isPermaLink="false">3331830</guid>        </item>
        <item>
            <title>The antitumor effect of PLK1 and HSF1 double knockdown on human oral carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3331829&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%3D20198330%26dopt%3DAbstract</link>
            <description>Authors: Kim SA, Kwon SM, Yoon JH, Ahn SG
    High levels of mitotic progression-associated PLK1 and stress-associated HSF1 have been observed in various human cancers. In the present study, we investigated the effects of PLK1 and HSF1 knockdown on the proliferation of oral cancer cells using small interfering RNA. In human oral squamous cell carcinoma (SCC) tissues, the levels of PLK1 and HSF1 were higher compared to normal tissues. The expression levels of PLK1 and HSF1 were also elevated in the human oral SCC cell lines FaDu and HEp-2. Disruption of PLK1 induced cell cycle arrest at G2/M phase as well as apoptosis in oral cancer cells. Interestingly, knockdown of both PLK1 and HSF1 expression decreased cell proliferation while increasing apoptotic cell death in synergistic fashion. Thes...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331829</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:14 +0100</pubDate>
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        <item>
            <title>Targeting the cell cycle and the PI3K pathway: A possible universal strategy to reactivate innate tumor suppressor programmes in cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3331828&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%3D20198331%26dopt%3DAbstract</link>
            <description>Authors: David-Pfeuty T, Legraverend M, Ludwig O, Grierson DS
    Corruption of the Rb and p53 pathways occurs in virtually all human cancers. This could be because it lends oncogene-bearing cells a surfeit of Cdk activity and growth, enabling them to elaborate strategies to evade tumor-suppressive mechanisms and divide inappropriately. Targeting both Cdk activities and the PI3K pathway might be therefore a potentially universal means to palliate their deficiency in cancer cells. We showed that the killing efficacy of roscovitine and 16 other purines and potentiation of roscovitine-induced apoptosis by the PI3K inhibitor, LY294002, decreased with increasing corruption of the Rb and p53 pathways. Further, we showed that purines differing by a single substitution, which exerted little lethal...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331828</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:11 +0100</pubDate>
            <guid isPermaLink="false">3331828</guid>        </item>
        <item>
            <title>PKCepsilon induces Bcl-2 by activating CREB.</title>
            <link>http://www.medworm.com/index.php?rid=3331827&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%3D20198332%26dopt%3DAbstract</link>
            <description>The objective of our present study was to determine the mode of induction of Bcl-2 by PKCepsilon in breast cancer cells. siRNA silencing of either PKCepsilon or Akt in MCF-7 cells, which overexpress Akt, decreased Bcl-2 protein and mRNA levels. However, knockdown of PKCepsilon, but not Akt, led to the decrease in Bcl-2 at both protein and mRNA levels in MDA-MB-231 breast cancer cells, which overexpress PKCepsilon but contain little constitutively-active Akt. Knockdown of PKCepsilon decreased phosphorylation of cAMP response element-binding protein (CREB) at Ser133 in MDA-MB-231 cells, and depletion of CREB by siRNA decreased Bcl-2 at both the protein and mRNA levels. In addition, knockdown of CREB sensitized MDA-MB-231 cells to TRAIL-mediated cell death. These results suggest that PKCepsil...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331827</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:08 +0100</pubDate>
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        <item>
            <title>Immunohistochemical profiling of node negative breast carcinomas allows prediction of metastatic risk.</title>
            <link>http://www.medworm.com/index.php?rid=3331826&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%3D20198333%26dopt%3DAbstract</link>
            <description>Authors: Giusiano S, Secq V, Carcopino X, Carpentier S, Andrac L, Lavaut MN, Allasia C, Bonnier P, Iovanna JL, Garcia S, Boubli L, Birnbaum D, Charpin C
    The aim of this study was to identify a prognostic immunohistochemical signature indicative of risk of early metastasis in node-negative breast carcinomas that would also be relevant to the development of new tailored therapy. Quantitative measurements of the immunohistochemical expression of 64 markers (selected from literature data) using high-throughput densitometry (as a continuous variable) of digitised microscopic micro-array images were correlated with clinical outcome in 667 node-negative breast carcinomas (mean follow-up 102 months). Multivariable fractional polynomials model of logistic regression allowed the selection of the...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331826</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:04 +0100</pubDate>
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        <item>
            <title>Overexpression of Apg-2 increases cell proliferation and protects from oxidative damage in BaF3-BCR/ABL cells.</title>
            <link>http://www.medworm.com/index.php?rid=3331825&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%3D20198334%26dopt%3DAbstract</link>
            <description>Authors: Li C, Liu D, Yuan Y, Huang S, Shi M, Tao K, Feng W
    Apg-2, a mammalian heat-shock protein belonging to the heat-shock protein 110 (Hsp110) family, was previously found to be overexpressed in BaF3-BCR/ABL cells that were treated with hydrogen peroxide (H2O2) through our comparative proteomics study. The expression of Apg-2 in chronic myelogenous leukemia (CML) cells and its role have not been investigated, forming the basis for this study. BaF3-MIGR1 and BaF3-BCR/ABL cell lines stably overexpressing Apg-2 were established and exposed to 50 microM H2O2 for 10 min. Western blot analysis of Apg-2 expression confirmed that H2O2 treatment significantly up-regulated Apg-2 expression. Apg-2 overexpression elevated BaF3-BCR/ABL cell proportions in S and G2/M phase, increased cell prolif...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331825</comments>
            <pubDate>Thu, 04 Mar 2010 22:59:00 +0100</pubDate>
            <guid isPermaLink="false">3331825</guid>        </item>
        <item>
            <title>A new system for regulated functional gene expression for gene therapy applications: Nuclear delivery of a p16INK4A-estrogen receptor carboxy terminal fusion protein only in the presence of estrogen.</title>
            <link>http://www.medworm.com/index.php?rid=3331824&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%3D20198335%26dopt%3DAbstract</link>
            <description>Authors: Tamura T, Kanuma T, Nakazato T, Faried LS, Aoki H, Minegishi T
    The clinical use of gene therapy requires tight regulation of the gene of interest and functional expression only when it is needed. Thus, it is necessary to develop ways of regulating functional gene expression with exogenous stimuli. Many regulatable systems are currently under development. For example, the tetracycline-dependent transcriptional switch has been successfully employed for in vivo preclinical applications. However, there are no examples of regulatable systems that have been employed in human clinical trials. In the present study, we established an adenovirus-delivered functional gene expression system that is regulated by estrogen. This system uses p16INK4A fused at its C-terminus to the ligand-bind...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331824</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:57 +0100</pubDate>
            <guid isPermaLink="false">3331824</guid>        </item>
        <item>
            <title>miR-221/222 promote malignant progression of glioma through activation of the Akt pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3331823&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%3D20198336%26dopt%3DAbstract</link>
            <description>In this study, we aimed to explore the coordinated function of miR-221/222 in glioma by bioinformatics and experiment methods. Bioinformatics analysis revealed that miR-221/222 had the potential to regulate about 70 common target genes and may exert a cooperative effect on regulation and function via Akt signaling pathway. Overexpression of miR-221/222 increased glioma cell proliferation and invasion in vitro and induced glioma growth in a subcutaneous mouse model. Furthermore, miR-221/222 overexpression resulted in an obvious activation of p-Akt and significant changes of Akt-related gene expression in glioma cells. Our results suggest that miR-221/222 co-enhance the glioma malignant phenotype via activation of the Akt pathway mediated by regulation of common gene expression.
    PMID: 20...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331823</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:53 +0100</pubDate>
            <guid isPermaLink="false">3331823</guid>        </item>
        <item>
            <title>17beta-estradiol induces up-regulation of PTEN and PPARgamma in leiomyoma cells, but not in normal cells.</title>
            <link>http://www.medworm.com/index.php?rid=3331822&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%3D20198337%26dopt%3DAbstract</link>
            <description>This report shows the first evidence that PTEN and PPARgamma are up-regulated in leiomyoma tissues, and estrogen stimulates expression of PTEN and PPARgamma in leiomyoma cells, but not in normal cells.
    PMID: 20198337 [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=3331822</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:50 +0100</pubDate>
            <guid isPermaLink="false">3331822</guid>        </item>
        <item>
            <title>Global screening and extended nomenclature for 230 aphidicolin-inducible fragile sites, including 61 yet unreported ones.</title>
            <link>http://www.medworm.com/index.php?rid=3331821&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%3D20198338%26dopt%3DAbstract</link>
            <description>Authors: Mrasek K, Schoder C, Teichmann AC, Behr K, Franze B, Wilhelm K, Blaurock N, Claussen U, Liehr T, Weise A
    Since the first description of human fragile sites (FS) more than 40 years ago, a variety of substances were reported to induce chromosomal breaks at non-random, breakage-prone regions. According to information available from human genome browsers aphidicolin, an inhibitor of DNA replication induces 77 of 88 known common FS. However, in the literature additional FS are reported, which are also, at least in part, inducible by aphidicolin. To the best of our knowledge, here we present the first and largest ever done systematic, whole genome-directed and comprehensive screening for aphidicolin-inducible breakage-prone regions. The study was performed on stimulated peripheral b...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331821</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:47 +0100</pubDate>
            <guid isPermaLink="false">3331821</guid>        </item>
        <item>
            <title>Bile acid regulates MUC2 transcription in colon cancer cells via positive EGFR/PKC/Ras/ERK/CREB, PI3K/Akt/IkappaB/NF-kappaB and p38/MSK1/CREB pathways and negative JNK/c-Jun/AP-1 pathway.</title>
            <link>http://www.medworm.com/index.php?rid=3331820&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%3D20198339%26dopt%3DAbstract</link>
            <description>Authors: Lee HY, Crawley S, Hokari R, Kwon S, Kim YS
    MUC2 is a major secretory mucin normally expressed by goblet cells of the intestine, but is aberrantly expressed in colonic neoplasia. Bile acids have been implicated in colorectal carcinogenesis and, therefore, we sought to determine the effects of bile acids on MUC2 expression and regulation in colon cancer cells. Since deoxycholic acid (DCA), a secondary bile acid, has been reported to be a potent mucin secretagogue and tumor promoter, DCA-treated HM3 colon cancer cells were analyzed using promoter-reporter assays of the 5' flanking region of the MUC2 gene. Chemical inhibitors, mutant reporter constructs and EMSA showed that DCA upregulates MUC2 transcription via multiple pathways involving activation of EGFR/PKC/Ras/Raf-1/MEK1/ER...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331820</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:44 +0100</pubDate>
            <guid isPermaLink="false">3331820</guid>        </item>
        <item>
            <title>SIRT3 SNPs validation in 640 individuals, functional analyses and new insights into SIRT3 stability.</title>
            <link>http://www.medworm.com/index.php?rid=3331819&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%3D20198340%26dopt%3DAbstract</link>
            <description>Authors: Dransfeld CL, Alborzinia H, W&amp;#xF6;lfl S, Mahlknecht U
    Sirtuins are critical players within multiple cellular pathways such as stress response, apoptosis and energy metabolism. They are associated with metabolic and degenerative diseases, the pathogenesis of cancer and are key elements in the regulation of cellular life span. From within the 7 known human sirtuins, SIRT3 recently stepped out of the shadow of SIRT1 showing strong effects on stress response, apoptosis, cell cycle and energy metabolism, mimicking effects of caloric restriction. We have identified two non-synonymous human SIRT3 SNPs and evaluated their impact on SIRT3 activity and stability. We assessed their influence on cellular energy metabolism in relation to SIRT1 and identified SIRT3 to increase cellular res...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331819</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:41 +0100</pubDate>
            <guid isPermaLink="false">3331819</guid>        </item>
        <item>
            <title>Isostrychnopentamine, an indolomonoterpenic alkaloid from Strychnos usambarensis, with potential anti-tumor activity against apoptosis-resistant cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3331818&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%3D20198341%26dopt%3DAbstract</link>
            <description>Authors: Saidou Balde el-H, M&amp;#xE9;galizzi V, Cao M, Angenot L, Kiss R, Van Damme M, Frederich M
    Isostrychnopentamine (ISP) is an indolomonoter-penic alkaloid that is present in the leaves of Strychnos usambarensis, an East African small tree. We have reported previously pro-apoptotic effects induced in vitro by ISP in the human HCT-116 colon cancer cell line, a model that displays relative sensitivity to apoptosis. In the present study, we observed that the in vitro growth inhibitory activities of ISP are similar in cancer cells that display sensitivity versus resistance to apoptosis. We made use of the U373 glioblastoma and the A549 non-small cell lung cancer (NSCLC) cell lines as models relatively resistant to apoptosis, and the human PC-3 prostate cancer cell line as a model relati...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331818</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:38 +0100</pubDate>
            <guid isPermaLink="false">3331818</guid>        </item>
        <item>
            <title>Effects of an EGFR-binding affibody molecule on intracellular signaling pathways.</title>
            <link>http://www.medworm.com/index.php?rid=3331817&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%3D20198342%26dopt%3DAbstract</link>
            <description>Authors: Nordberg E, Ekerljung L, Sahlberg SH, Carlsson J, Lennartsson J, Glimelius B
    Effects on intracellular signaling were studied in cells treated with the affibody molecule (ZEGFR:955)2 that targets the epithelial growth factor receptor (EGFR). EGFR is overexpressed in many types of cancers and plays a fundamental role in cell signaling and it is of interest to find targeting agents capable of blocking the receptor. The clinically approved antibody cetuximab (Erbitux(R)) and the natural ligand EGF were included as reference molecules. Two EGFR-rich cell lines, A-431 and U-343, were exposed to the three targeting agents and lysed. The cell lysates were immunoprecipitated with the receptors, or directly separated by SDS-Page. Autophosphorylation of the receptors and phosphorylation ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331817</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:33 +0100</pubDate>
            <guid isPermaLink="false">3331817</guid>        </item>
        <item>
            <title>Mass spectrometric detection of candidate protein biomarkers of cancer cachexia in human urine.</title>
            <link>http://www.medworm.com/index.php?rid=3331816&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%3D20198343%26dopt%3DAbstract</link>
            <description>Authors: Skipworth RJ, Stewart GD, Bhana M, Christie J, Sturgeon CM, Guttridge DC, Cronshaw AD, Fearon KC, Ross JA
    Increased membrane permeability and myofibrillar protein breakdown are established features of cancer cachexia. Proteins released from cachectic muscle may be excreted in urine to act as biomarkers of the cachectic process. One-dimensional SDS polyacrylamide gel electrophoresis followed by matrix-assisted laser desorption/ionisation or liquid chromatography tandem mass spectrometry was used to compare the protein content of urine from cachectic (&amp;gt;10% weight loss) (n=8) and weight-stable (n=8) gastro-oesophageal cancer patients and healthy controls (n=8). Plasma creatine kinase concentration was used as a marker of gross muscle breakdown. The number of protein species id...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331816</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:30 +0100</pubDate>
            <guid isPermaLink="false">3331816</guid>        </item>
        <item>
            <title>Heterozygous TP53stop146/R72P fibroblasts from a Li-Fraumeni syndrome patient with impaired response to DNA damage.</title>
            <link>http://www.medworm.com/index.php?rid=3331815&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%3D20198344%26dopt%3DAbstract</link>
            <description>Authors: De Moura J, Kavalec FL, Doghman M, Rosati R, Custodio G, Lalli E, Cavallari GM, Santa Maria J, Figueiredo BC
    The Li-Fraumeni syndrome (LFS) is a rare autosomal dominant hereditary cancer syndrome, characterized by a wide spectrum of neoplasms, occurring in children and young adults. The identification of germline TP53 mutations in LFS has given rise to a number of in vitro studies using cultures of cancer cells and non-tumoral fibroblasts presenting germline TP53 mutations. In the present study, we performed a detailed documentation of the pedigree of an LFS family with a comprehensive analysis of genotype-phenotype correlations. We sequenced the TP53 gene and verified that the proband carries a germline nonsense mutation in codon 146 in one allele, the TP53Arg72Pro polymorphi...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331815</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:26 +0100</pubDate>
            <guid isPermaLink="false">3331815</guid>        </item>
        <item>
            <title>The cell cycle effects of docosahexaenoic acid on human metastatic hepatocellular carcinoma proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=3331814&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%3D20198345%26dopt%3DAbstract</link>
            <description>This study provides novel mechanistic insights into the modulation of DHA on human hepatocarcinoma.
    PMID: 20198345 [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=3331814</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:23 +0100</pubDate>
            <guid isPermaLink="false">3331814</guid>        </item>
        <item>
            <title>Synergistic antineoplastic effect of DLC1 tumor suppressor protein and histone deacetylase inhibitor, suberoylanilide hydroxamic acid (SAHA), on prostate and liver cancer cells: Perspectives for therapeutics.</title>
            <link>http://www.medworm.com/index.php?rid=3331813&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%3D20198346%26dopt%3DAbstract</link>
            <description>Authors: Zhou X, Yang XY, Popescu NC
    Inactivation of tumor suppressor genes is a major contributing alteration in the initiation or progression of cancer. The human tumor suppressor gene DLC1 (deleted in liver cancer 1) is frequently downregulated or silenced in multiple cancers, predominantly by epigenetic mechanisms. With the current considerable interest and progress in epigenetic therapy, a number of promising antineoplastic agents, particularly histone deacetylase (HDAC) inhibitors, have been developed and used successfully in clinical trials. Both DLC1 and HDAC inhibitors exert antineoplastic functions, and their combined action could be exploited for a more effective cancer therapy. To evaluate the potential benefits of this approach, we examined the antineoplastic effects of ad...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331813</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:20 +0100</pubDate>
            <guid isPermaLink="false">3331813</guid>        </item>
        <item>
            <title>Differential effects of resveratrol and novel resveratrol derivative, HS-1793, on endoplasmic reticulum stress-mediated apoptosis and Akt inactivation.</title>
            <link>http://www.medworm.com/index.php?rid=3331812&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%3D20198347%26dopt%3DAbstract</link>
            <description>Authors: Um HJ, Bae JH, Park JW, Suh H, Jeong NY, Yoo YH, Kwon TK
    Since resveratrol (3,4',5 tri-hydroxystilbene), which has been shown to inhibit multistage carcinogenesis, is not a potent cytotoxic compound, several studies were undertaken to obtain synthetic analogues of resveratrol with potent activity. We previously reported that a resveratrol derivative HS-1793 exhibits stronger antitumor effects than resveratrol in several cancer cell types. The present study was undertaken to reveal precise mechanism by which HS-1793 induces cell death. The induction of CCAAT/enhancer-binding protein-homologous protein (CHOP) and glucose-regulated protein (GRP)-78, and ER stress-specific XBP1 splicing were found in HT29 human colon carcinoma cells treated with resveratrol. Conversely, these mani...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331812</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:17 +0100</pubDate>
            <guid isPermaLink="false">3331812</guid>        </item>
        <item>
            <title>Porcupine expression is associated with the expression of S100P and other cancer-related molecules in non-small cell lung carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3331811&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%3D20198348%26dopt%3DAbstract</link>
            <description>In conclusion, besides DNA methylation processes, Porcupine might regulate the expression of some cancer-related molecules including S100P in human NSCLC.
    PMID: 20198348 [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=3331811</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:14 +0100</pubDate>
            <guid isPermaLink="false">3331811</guid>        </item>
        <item>
            <title>Reovirus infection induces apoptosis of TRAIL-resistant gastric cancer cells by down-regulation of Akt activation.</title>
            <link>http://www.medworm.com/index.php?rid=3331810&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%3D20198349%26dopt%3DAbstract</link>
            <description>Authors: Cho IR, Koh SS, Min HJ, Park EH, Srisuttee R, Jhun BH, Kang CD, Kim M, Johnston RN, Chung YH
    The tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has been used to treat a variety of cancer cells. However, since some gastric cancer cells are resistant to TRAIL, we explored whether reovirus induces cytolysis in TRAIL-resistant gastric cancer cells. We found that TRAIL-resistant SNU-216 gastric cancer cells were susceptible to apoptosis by reovirus infection. Furthermore, co-treatment with reovirus and TRAIL accelerated apoptosis of SNU-216 cells by down-regulation of Akt activation as assessed by a very low activation of Akt in TRAIL-sensitive SNU-668 gastric cancer cells. Inhibition of Akt signaling with wortmannin or suppression of Akt expression with sh-A...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331810</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:11 +0100</pubDate>
            <guid isPermaLink="false">3331810</guid>        </item>
        <item>
            <title>Identification of a functional p53 responsive element within the promoter of XAF1 gene in gastrointestinal cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3331809&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%3D20198350%26dopt%3DAbstract</link>
            <description>In conclusion, we demonstrated that p53 could suppress the transcription of XAF1 through interaction with a high affinity responsive element (-95 to -86 nt) within XAF1 promoter, indicating a novel exclusive mechanism between these two tumor suppressors.
    PMID: 20198350 [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=3331809</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:08 +0100</pubDate>
            <guid isPermaLink="false">3331809</guid>        </item>
        <item>
            <title>Increase of the therapeutic effect by treating nasopharyngeal tumor with combination of HER-2 siRNA and paclitaxel.</title>
            <link>http://www.medworm.com/index.php?rid=3331808&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%3D20198351%26dopt%3DAbstract</link>
            <description>In this study, we investigated antitumor activity by RNA interference in combination with paclitaxel (PTX) for KB cells using HER-2 siRNA and HER-2 short hairpin RNA-expressing plasmid DNA (HER-2 shRNA pDNA). Suppression of HER-2 expression by siRNA or shRNA pDNA caused significant reduction of proliferation by inducing apoptosis and enhancing the sensitivity for PTX in HER-2 positive KB cells. Interestingly, an HER-2 antibody trastuzumab could not increase the antitumor effect by PTX in KB xenografts. Combination therapy by intratumoral injection of HER-2 siRNA or HER-2 shRNA pDNA with PTX significantly inhibited the tumor growth of xenografts compared with each therapy used individually. In particular, HER-2 shRNA pDNA plus PTX largely extended the mean survival days compared with HER-2 ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3331808</comments>
            <pubDate>Thu, 04 Mar 2010 22:58:05 +0100</pubDate>
            <guid isPermaLink="false">3331808</guid>        </item>
        <item>
            <title>Gene alterations in head and neck carcinomas and their role in promoting malignant behavior (Review).</title>
            <link>http://www.medworm.com/index.php?rid=3240053&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%3D20126971%26dopt%3DAbstract</link>
            <description>This article reviews literature on the current understanding of molecular HNSCC carcinogenesis, and highlights the most promising therapeutic approaches.
    PMID: 20126971 [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=3240053</comments>
            <pubDate>Thu, 04 Feb 2010 21:23:12 +0100</pubDate>
            <guid isPermaLink="false">3240053</guid>        </item>
        <item>
            <title>Timing of surgery and radiotherapy in the management of metastatic spine disease: A systematic review.</title>
            <link>http://www.medworm.com/index.php?rid=3240052&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%3D20126972%26dopt%3DAbstract</link>
            <description>Authors: Itshayek E, Yamada J, Bilsky M, Schmidt M, Shaffrey C, Gerszten P, Polly D, Gokaslan Z, Varga PP, Fisher CG
    The last decade has witnessed a dramatic change in management of metastatic spine disease, with an increased role for surgery and emerging use of stereotactic radiotherapy, often in combination. Patients may be treated with radiotherapy followed by surgery, or have surgery and then adjuvant radiotherapy. In both cases, the surgeon and oncologist need to select the optimal timing for surgery and radiotherapy to minimize wound complications while obtaining maximum oncolytic effects. The purpose of this review was to determine the optimal timing of surgery and radiotherapy in patients surgically treated for spinal metastases. A systematic review utilizing Medline, Embase, P...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240052</comments>
            <pubDate>Thu, 04 Feb 2010 21:23:10 +0100</pubDate>
            <guid isPermaLink="false">3240052</guid>        </item>
        <item>
            <title>Induction of protective immunity against MHC class I-deficient, HPV16-associated tumours with peptide and dendritic cell-based vaccines.</title>
            <link>http://www.medworm.com/index.php?rid=3240051&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%3D20126973%26dopt%3DAbstract</link>
            <description>In this study, we investigated the efficacy of prophylactic peptide and peptide-pulsed dendritic cell-based vaccines in a murine model of experimental MHC class I-deficient tumours (TC-1/A9), expressing E6/E7 oncogenes derived from HPV16, and compared the efficacy of particular vaccination settings to anti-tumour protection against parental MHC class I-positive TC-1 tumours. Peptide vaccine based on the 'short' peptide E749-57 harbouring solely the CTL epitope and co-administered to the C57BL/6 mice with CpG oligodeoxynucleotide (CpG ODN) 1826 was effective against MHC class I-positive but not -deficient tumours, while the 'longer' peptide E744-62 (peptide 8Q, harbouring CTL and Th epitopes)-based vaccines were also effective against MHC class I-deficient tumours. We have compared the adju...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240051</comments>
            <pubDate>Thu, 04 Feb 2010 21:23:07 +0100</pubDate>
            <guid isPermaLink="false">3240051</guid>        </item>
        <item>
            <title>The pure anti-androgen bicalutamide inhibits cyclin A expression both in androgen-dependent and -independent cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=3240050&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%3D20126974%26dopt%3DAbstract</link>
            <description>Authors: Katayama H, Murashima T, Saeki Y, Nishizawa Y
    We investigated the effects of testosterone and the pure anti-androgen, bicalutamide, on DNA synthesis and cell cycle in androgen-sensitive or -insensitive human and mouse cell lines by 3H-thymidine incorporation, flow cytometry, RT-PCR and Western blotting. In androgen-dependent mouse SC-3 cells, testosterone induced DNA synthesis, shift of cell cycle distribution from G0/G1 to S/G2/M and expression of cyclin A. The induction was preceded by that of fibroblast growth factor 8 (FGF-8), and completely blocked by monoclonal antibody to FGF-8. Dihydrotestosterone (DHT) induced cyclin A expression in androgen-sensitive human prostate cancer cells, but not in androgen-independent cell lines. Bicalutamide almost completely inhibited thes...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240050</comments>
            <pubDate>Thu, 04 Feb 2010 21:23:04 +0100</pubDate>
            <guid isPermaLink="false">3240050</guid>        </item>
        <item>
            <title>TDGF1 is a novel predictive marker for metachronous metastasis of colorectal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3240049&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%3D20126975%26dopt%3DAbstract</link>
            <description>In conclusion, the present data strongly suggest the usefulness of TDGF1 as a predictive marker for metachronous metastasis in CRC patients.
    PMID: 20126975 [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=3240049</comments>
            <pubDate>Thu, 04 Feb 2010 21:23:02 +0100</pubDate>
            <guid isPermaLink="false">3240049</guid>        </item>
        <item>
            <title>Overexpression of SUGT1 in human colorectal cancer and its clinicopathological significance.</title>
            <link>http://www.medworm.com/index.php?rid=3240048&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%3D20126976%26dopt%3DAbstract</link>
            <description>Authors: Iwatsuki M, Mimori K, Sato T, Toh H, Yokobori T, Tanaka F, Ishikawa K, Baba H, Mori M
    As recent technological innovations make it possible to clarify the concordant relationship between genomic alterations and aberrant gene expression during the progression of colorectal cancer (CRC), we aimed at identifying new overexpressing genes with genomic amplification on the responsible loci in CRC. The candidate gene was found using cDNA microarray and array-based comparative genomic hybridization (CGH) analysis after laser microdissection (LMD) in 132 Japanese CRC. We focused on SUGT1, which is associated with the assembling of kinetochore proteins at the metaphase of the cell cycle, with significant association between genetic alterations and expression. SUGT1 mRNA expression was ev...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240048</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:59 +0100</pubDate>
            <guid isPermaLink="false">3240048</guid>        </item>
        <item>
            <title>Enhancement of human cancer cell radiosensitivity by conjugated eicosapentaenoic acid - a mammalian DNA polymerase inhibitor.</title>
            <link>http://www.medworm.com/index.php?rid=3240047&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%3D20126977%26dopt%3DAbstract</link>
            <description>Authors: Kumamoto-Yonezawa Y, Sasaki R, Suzuki Y, Matsui Y, Hada T, Uryu K, Sugimura K, Yoshida H, Mizushina Y
    We previously found that conjugated eicosapentaenoic acid (cEPA) selectively inhibited the activities of mammalian DNA polymerases (pols), and suppressed human cancer cell growth. The aim of the present study was to evaluate the efficacy of concurrent radiation with cEPA in a human colon carcinoma cell line, HCT 116. Furthermore, we examined the most effective timing of irradiation. The post-irradiation addition of cEPA significantly enhanced HCT116 cell radiosensitivity by decreasing the expression of pols beta, delta and epsilon, increasing damaged DNA, such as DNA double-strand breaks, inhibiting clonogenic survival, and inducing apoptosis. However, cells treated by pre-irr...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240047</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:55 +0100</pubDate>
            <guid isPermaLink="false">3240047</guid>        </item>
        <item>
            <title>Rho-kinase regulates negatively the epidermal growth factor-stimulated colon cancer cell proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=3240046&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%3D20126978%26dopt%3DAbstract</link>
            <description>In this study, we investigated the role of Rho-kinase in epidermal growth factor (EGF) signaling in SW480 colon cancer cells. We found that Y27632, a Rho-kinase inhibitor, dose-dependently induced cell proliferation in these cells. The blockade of EGF stimulation utilizing anti-EGF receptor neutralizing antibodies significantly suppressed cell growth, suggesting that EGF stimulation plays an important role in cell proliferation in SW480 cells. We also found that EGF induced Rho-kinase activation. Interestingly, EGF-induced phosphorylation of both Akt and glycogen synthase kinase-3beta (GSK-3beta), but not p44/p42 mitogen-activated protein (MAP) kinase, were dose-dependently enhanced when the cells were pretreated with Y27632 or fasudil, another Rho-kinase inhibitor. Moreover, whereas EGF i...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240046</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:53 +0100</pubDate>
            <guid isPermaLink="false">3240046</guid>        </item>
        <item>
            <title>PSK enhances the efficacy of docetaxel in human gastric cancer cells through inhibition of nuclear factor-kappaB activation and survivin expression.</title>
            <link>http://www.medworm.com/index.php?rid=3240045&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%3D20126979%26dopt%3DAbstract</link>
            <description>Authors: Kinoshita J, Fushida S, Harada S, Makino I, Nakamura K, Oyama K, Fujita H, Ninomiya I, Fujimura T, Kayahara M, Ohta T
    Docetaxel, a member of the taxane family, induces antitumor effects in patients with advanced gastric cancer. However, toxicity at therapeutic doses can be severe, resulting in discontinuation of therapy. It is possible that dose reduction due to adverse events may decrease the cytotoxic efficacy of docetaxel. PSK, a protein-bound polysaccharide, has been used as a chemoimmunotherapy agent in the treatment of cancer in Asia for over 30 years. In the present study, we investigated the enhancing effects of PSK on the cytotoxicity of docetaxel in human gastric cancer through non-immunological actions both in vitro and in vivo. The sensitization effects of PSK on d...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240045</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:50 +0100</pubDate>
            <guid isPermaLink="false">3240045</guid>        </item>
        <item>
            <title>Older versus younger patients with metastatic adenocarcinoma of the esophagus, gastroesophageal junction, and stomach: A pooled analysis of eight consecutive North Central Cancer Treatment Group (NCCTG) trials.</title>
            <link>http://www.medworm.com/index.php?rid=3240044&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%3D20126980%26dopt%3DAbstract</link>
            <description>Authors: Jatoi A, Foster NR, Egner JR, Burch PA, Stella PJ, Rubin J, Dakhil SR, Sargent DJ, Murphy BR, Alberts SR
    Whether elderly patients with metastatic esophageal, gastroesophageal, and gastric cancer do as well with chemotherapy as their younger counterparts was investigated in this pooled analysis. In total, 367 patients from 8 consecutive, first-line trials were included: i) etoposide + cisplatin; ii) 5-fluorourucil + leucovorin; iii) 5-fluorouracil + levamisole; iv) irinotecan; v) docetaxel + irinotecan; vi) oxaliplatin + capecitabine; vii) docetaxel + capecitabine; and viii) bortezomib + paclitaxel + carboplatin. One hundred and fifty-four (42%) patients were &amp;gt;/=65 years old (range: 65-86), and 213 younger (range: 20-64). Elderly patients had worse performance scores (2-3): ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240044</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:47 +0100</pubDate>
            <guid isPermaLink="false">3240044</guid>        </item>
        <item>
            <title>A population-based gene signature is predictive of breast cancer survival and chemoresponse.</title>
            <link>http://www.medworm.com/index.php?rid=3240043&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%3D20126981%26dopt%3DAbstract</link>
            <description>This study sought to develop a prognostic scheme based on a 28-gene signature in a broad patient population, including those with advanced disease. Clinically annotated transcriptional profiles of 1,734 breast cancer patients were obtained to validate the 28-gene signature in prognostic categorization. The 28-gene signature generated significant patient stratification with regard to breast cancer disease-free survival (log-rank P&amp;lt;0.0001; n=1,337) and overall survival (log-rank P&amp;lt;0.0001; n=806) in Kaplan-Meier analyses. The gene expression signature provides refined prognosis of disease-free survival (log-rank P&amp;lt;0.006; Kaplan-Meier analysis) within each classic clinicopathologic factor-defined subgroup, including LN-, LN+, ER-, ER+ and tumor grade II. Furthermore, it was investigat...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240043</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:44 +0100</pubDate>
            <guid isPermaLink="false">3240043</guid>        </item>
        <item>
            <title>Cryotreatment as a simple method for cell preparation in autologous tumor cell-based vaccination.</title>
            <link>http://www.medworm.com/index.php?rid=3240042&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%3D20126982%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated that a preparation containing cryotreated human breast cancer cells has the same capacity as a preparation containing irradiated human breast cancer cells to induce the activation of immune cells in vivo. The vaccine strategy proposed in this study may provide the experiment basis for the use of autologous or allogeneic breast cancer cells in the cell-based vaccine approach for the treatment of breast cancer and other types of cancer as well.
    PMID: 20126982 [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=3240042</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:42 +0100</pubDate>
            <guid isPermaLink="false">3240042</guid>        </item>
        <item>
            <title>The molecular mechanism of Vav3 oncogene on upregulation of androgen receptor activity in prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3240041&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%3D20126983%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Wu X, Dong Z, Lu S
    Our previous studies revealed that Vav3 oncogene is overexpressed in human prostate cancer, enhances androgen receptor (AR)-mediated signaling, and may play a role in prostate cancer development and progression. The purpose of this study was to determine the molecular mechanisms responsible for AR activation by Vav3. We found that interaction between N-terminus and C-terminus of AR is essential for its elevated activity stimulated by Vav3. The DH and PH domains of Vav3 are involved in direct interaction with AR. Both cytoplasmic and nuclear levels of AR and Vav3 are elevated and their nuclear localization is further stimulated by DHT in androgen-independent LNCaP-AI cells relative to their parental androgen-dependent LNCaP cells. Vav3 is colocalized w...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240041</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:39 +0100</pubDate>
            <guid isPermaLink="false">3240041</guid>        </item>
        <item>
            <title>Secreted form of EphA7 in lung cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3240040&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%3D20126984%26dopt%3DAbstract</link>
            <description>We report here a novel spliced variant, the so-called secreted form of EPHA7, recently reported in malignant lymphoma, in human lung cancer cell lines and primary lung cancer. In contrast to the EPHA7 down-regulation in colorectal cancer by promoter hypermethylation, EPHA7 is expressed at a substantial level in most human lung cancers and the secreted form of EPHA7 mRNA was found in a fraction of primary lung cancer tissues, lung cancer cell lines, and immortalized bronchogenic epithelial cell lines. Interestingly, the secreted form of EPHA7 message was predominantly detected in non-adeno type lung carcinoma. The mechanistic role of the secreted form of EPHA7 in human lung carcinogenesis is not clear, but the presence of this form could distinctly exclude adenocarcinoma of the lung from th...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240040</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:36 +0100</pubDate>
            <guid isPermaLink="false">3240040</guid>        </item>
        <item>
            <title>2-Aminophenoxazine-3-one induces cellular apoptosis by causing rapid intracellular acidification and generating reactive oxygen species in human lung adenocarcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3240039&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%3D20126985%26dopt%3DAbstract</link>
            <description>Authors: Zheng CL, Che XF, Akiyama S, Miyazawa K, Tomoda A
    2-Aminophenoxazine-3-one (Phx-3)-induced apoptosis was investigated. Phx-3 suppressed the viability of human lung adenocarcinoma cell line A549 and induced cellular apoptosis 6 h after treatment. Prior to these events, intracellular pH (pHi) was rapidly decreased from pH 7.65 to 7.10 within 30 min when A549 cells were treated with 7 microM Phx-3. This intracellular acidification continued for 3 h in the cells. Augmented production of reactive oxygen species (ROS) was obseved 1 h after treatment of A549 cells with 7 microM Phx-3, and cell cycle arrest at G1 was indicated 3 h after treatment. The translocation of NF-kappaB from the cytosol to the nucleus was clearly indicated 1 h after the administration of Phx-3 to A549 cells, w...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240039</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:34 +0100</pubDate>
            <guid isPermaLink="false">3240039</guid>        </item>
        <item>
            <title>Expression level of Pre B cell leukemia homeobox 2 correlates with poor prognosis of gastric adenocarcinoma and esophageal squamous cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3240038&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%3D20126986%26dopt%3DAbstract</link>
            <description>Authors: Qiu Y, Song B, Zhao G, Deng B, Makino T, Tomita Y, Wang J, Luo W, Doki Y, Aozasa K, Morii E
    Pre B cell leukemia homeobox 2 (PBX2), a member of PBX family, acts as a co-factor of homeobox proteins to regulate proliferation and differentiation of tumor cells. Our recent study revealed prognostic significance of PBX2 expression in non-small cell lung carcinoma. The significance of PBX2 expression was examined in cases with gastric cancer (GC) and esophageal squamous cell carcinoma (ESCC), and the role of PBX2 in tumor behavior was evaluated in GC and ESCC cell lines of knocked-down PBX2 expression. Expression level of PBX2 was immunohistochemically examined in 94 patients of GC and 64 patients of ESCC. Staining intensity for PBX2 was categorized as equal to or stronger (level 1) ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240038</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:31 +0100</pubDate>
            <guid isPermaLink="false">3240038</guid>        </item>
        <item>
            <title>Role of the AKT pathway in microRNA expression of human U251 glioblastoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3240037&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%3D20126987%26dopt%3DAbstract</link>
            <description>Authors: Zhou X, Ren Y, Han L, Mei M, Xu P, Zhang CZ, Wang GX, Jia ZF, Pu PY, Kang CS
    Activation of the AKT (serine-threonine kinase) pathway is a common feature in glioblastoma cells. Downstream factors of the AKT pathway are involved in cell proliferation, apoptosis, cellular migration and angiogenesis. Micro-RNAs (miRNAs) are highly conserved small non-coding RNAs that block targeted mRNA expression at the post-transcriptional level. The aim of this study was to investigate the role of the AKT pathway in regulating miRNA. The changes of miRNA expression profile in human glioblastome U251 cells after AKT small interfering RNA transfection were examined by a microarray, and confirmed by Northern blotting. Down-regulation of AKT expression by siRNA decreased the activity of AKT pathway...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240037</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:29 +0100</pubDate>
            <guid isPermaLink="false">3240037</guid>        </item>
        <item>
            <title>Bioactivity and molecular targets of novel substituted quinolines in murine and human tumor cell lines in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3240036&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%3D20126988%26dopt%3DAbstract</link>
            <description>In conclusion, antiproliferative PQ1 is effective against a spectrum of tumor cells and might interact with various membrane and nuclear targets to enhance gap junctions, inhibit nucleoside transport and block cytokinesis but does not appear to disrupt the EGF receptor-mediated signaling pathways to induce growth arrest and apoptosis.
    PMID: 20126988 [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=3240036</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:24 +0100</pubDate>
            <guid isPermaLink="false">3240036</guid>        </item>
        <item>
            <title>REG4 acts as a mitogenic, motility and pro-invasive factor for colon cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3240035&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%3D20126989%26dopt%3DAbstract</link>
            <description>Authors: Rafa L, Dessein AF, Devisme L, Buob D, Truant S, Porchet N, Huet G, Buisine MP, Lesuffleur T
    REG4, the latest member of the regenerating gene family, is overexpressed in inflammatory bowel diseases and gastrointestinal carcinomas. To date, its pathophysiologic role has not been well established. Using HT-29 models, we previously identified REG4 as being overexpressed in colorectal tumor cells displaying a drug-resistance phenotype; some also displayed invasive properties. Thus, we investigated the potential functions of REG4 in biological processes involved in colorectal tumor progression such as cell proliferation, migration and invasion. Colon cancer cells secreting REG4 (HT29-5M21, HT29-5F7 and HT29/REG4-8) or not (HT-29, HT29/CT1 and Caco-2/TC7) were used to analyze the au...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240035</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:22 +0100</pubDate>
            <guid isPermaLink="false">3240035</guid>        </item>
        <item>
            <title>Loss of the p53 tumor suppressor activity is associated with negative prognosis of mantle cell lymphoma.</title>
            <link>http://www.medworm.com/index.php?rid=3240034&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%3D20126990%26dopt%3DAbstract</link>
            <description>Authors: Stefancikova L, Moulis M, Fabian P, Ravcukova B, Vasova I, Muzik J, Malcikova J, Falkova I, Slovackova J, Smardova J
    Mantle cell lymphoma (MCL) is typified by translocation t(11;14)(q13;q32) causing upregulation of cyclin D1 and deregulation of cell cycle. The cyclin D1 activation plays a critical role in MCL pathogenesis but additional oncogenic events, such as aberrations of the ARF/MDM2/p53 pathway are also necessary for progression of the disease. We analyzed the p53 tumor suppressor in tumor tissue of 33 patients with MCL. The p53 status was determined by functional analyses in yeast (FASAY) and by cDNA sequencing. The level of the p53 protein was assessed by immunohistochemistry and immunoblotting. Loss of the p53-specific locus 17p13.3 was detected by FISH. Mutations in...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240034</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:19 +0100</pubDate>
            <guid isPermaLink="false">3240034</guid>        </item>
        <item>
            <title>Primary ovarian cancer cells are sensitive to the proaptotic effects of proteasome inhibitors.</title>
            <link>http://www.medworm.com/index.php?rid=3240033&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%3D20126991%26dopt%3DAbstract</link>
            <description>Authors: Pasquini L, Petronelli A, Petrucci E, Saulle E, Mariani G, Scambia G, Benedetti-Panici P, Greggi S, Cognetti F, Testa U
    Resistance of tumors to cell death signals poses a complex clinical problem. In the present study, we have explored the capacity of proteasome inhibitors to induce cell death of ovarian cancer cells. We explored the sensitivity of primary ovarian cancer cells to a combination of bortezomib (also known as PS-341), a proteasome inhibitor and TRAIL, a death ligand, or mapatumumab or lexatumumab, TRAIL-R1 or TRAIL-R2 targeting agonist monoclonal antibodies, respectively. The results of our study showed that the large majority of primary ovarian cancers are clearly sensitive to the pro-apoptotic action of bortezomib, whose effects are potentiated by the concomitan...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240033</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:16 +0100</pubDate>
            <guid isPermaLink="false">3240033</guid>        </item>
        <item>
            <title>Chronologic aging decreases tumor angiogenesis and metastasis in a mouse model of head and neck cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3240032&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%3D20126992%26dopt%3DAbstract</link>
            <description>We examined the effects of aging on squamous cell carcinoma formation in a mouse model. Chronologically aged mice experience shorter tumor latency periods than wild-type animals. Tumors in aged mice were poorly vascularized, necrotic, and produced significantly fewer cervical lymph node metastases. Vascular endothelial growth factor expression was similar in primary tumors from young and old mice, but microvessel density was significantly reduced in tumors arising in aged mice. These results indicate that host response to angiogenic factors inhibit tumor growth and metastasis of head and neck cancer.
    PMID: 20126992 [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=3240032</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:13 +0100</pubDate>
            <guid isPermaLink="false">3240032</guid>        </item>
        <item>
            <title>Proteomic characterization of the cellular response to chemopreventive triterpenoid astragaloside IV in human hepatocellular carcinoma cell line HepG2.</title>
            <link>http://www.medworm.com/index.php?rid=3240031&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%3D20126993%26dopt%3DAbstract</link>
            <description>This study was designed to characterize the intracellular proteins regulated by astragaloside IV, the major active triterpenoid in Radix Astragali. Upon the treatment with astragaloside IV, human hepatocellular carcinoma HepG2 cells were evaluated for the colonogenic survival and anchorage-independent growth. The cellular proteins of treated and untreated cells were resolved by 2-D polyacrylamide gel electrophoresis. The protein spots mostly altered by drug treatment were identified by mass spectrometry and subsequently verified by Western blotting using specific antibodies and RT-PCR technique using specific DNA primers. We found that astragaloside IV attenuated the colonogenic survival and anchorage-independent growth of cancer cells. Based on the proteomic profiles, top 14 upregulated a...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240031</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:11 +0100</pubDate>
            <guid isPermaLink="false">3240031</guid>        </item>
        <item>
            <title>Docosahexaenoic acid intake decreases proliferation, increases apoptosis and decreases the invasive potential of the human breast carcinoma cell line MDA-MB-231.</title>
            <link>http://www.medworm.com/index.php?rid=3240030&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%3D20126994%26dopt%3DAbstract</link>
            <description>Authors: Blanckaert V, Ulmann L, Mimouni V, Antol J, Brancquart L, Ch&amp;#xE9;nais B
    Breast cancer is the most common cancer in women in industrialized countries. Environmental factors, such as differences in diet are likely to have an important influence on cancer emergence. Among these factors, n-3 polyunsaturated-fatty acids, such as docosahexaenoic acid (DHA), are good candidates for preventing breast cancer. Here we investigate the effect of DHA on the human breast cancer cell line MDA-MB-231 and show that DHA incorporation i) has an anti-proliferative effect, ii) induces apoptosis via a transient increase in caspase-3 activity and the promotion of nuclear condensation, and iii) reduces the invasive potential of MDA-MB-231 cells. To conclude, DHA may have beneficial effects as a resu...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240030</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:08 +0100</pubDate>
            <guid isPermaLink="false">3240030</guid>        </item>
        <item>
            <title>Diallylpolysulfides induce growth arrest and apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=3240029&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%3D20126995%26dopt%3DAbstract</link>
            <description>Authors: Busch C, Jacob C, Anwar A, Burkholz T, Aicha Ba L, Cerella C, Diederich M, Brandt W, Wessjohann L, Montenarh M
    Garlic-derived organo sulphur compounds such as diallylsulfides provide a significant protection against carcinogenesis. Chemically synthesized, and highly pure diallylsulfides with a chain of 1-4 sulphur atoms, as well as a range of control compounds, were employed to investigate the influence of these agents on cell viability, cell cycle arrest and induction of apoptosis in HCT116 human colon cancer cells. Diallyltrisulfide, and even more efficiently diallyltetrasulfide treatment of HCT116 cells led to a reduced cell viability, cell cycle arrest and apoptosis. A similar activity was found for the propyl-analogues, while mono- and disulfides were considerably less ac...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3240029</comments>
            <pubDate>Thu, 04 Feb 2010 21:22:06 +0100</pubDate>
            <guid isPermaLink="false">3240029</guid>        </item>
        <item>
            <title>High-resolution magic angle spinning magnetic resonance spectroscopy detects glycine as a biomarker in brain tumors.</title>
            <link>http://www.medworm.com/index.php?rid=3136093&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%3D20043062%26dopt%3DAbstract</link>
            <description>Authors: Righi V, Andronesi OC, Mintzopoulos D, Black PM, Tzika AA
    The non-essential amino acid neurotransmitter glycine (Gly) may serve as a biomarker for brain tumors. Using 36 biopsies from patients with brain tumors [12 glioblastoma multiforme (GBM); 10 low-grade (LG), including 7 schwannoma and 3 pylocytic astrocytoma; 7 meningioma (MN); 7 brain metastases (MT), including 3 adenocarcinoma and 4 breast cancer] and 9 control biopsies from patients undergoing surgery for epilepsy, we tested the hypothesis that the presence of glycine may distinguish among these brain tumor types. Using high-resolution magic angle spinning (HRMAS) 1H magnetic resonance spectroscopy (MRS), we determined a theoretically optimum echo time (TE) of 50 ms for distinguishing Gly signals from overlapping myo-...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136093</comments>
            <pubDate>Sat, 02 Jan 2010 08:49:17 +0100</pubDate>
            <guid isPermaLink="false">3136093</guid>        </item>
        <item>
            <title>New aspects on chromosomal instability: chromosomal break-points in Fanconi anemia patients co-localize on the molecular level with fragile sites.</title>
            <link>http://www.medworm.com/index.php?rid=3136092&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%3D20043063%26dopt%3DAbstract</link>
            <description>Authors: Schoder C, Liehr T, Velleuer E, Wilhelm K, Blaurock N, Weise A, Mrasek K
    Within cytogenetic preparations chromosomal breaks can be observed in patients suffering from Fanconi anemia (FA), a recessively inherited syndrome with an extremely elevated cancer risk, but also in healthy individuals as so-called fragile sites (FS). It is known that FS cytogenetically co-localize with tumor- and evolutionary-conserved chromosomal break-points. The also suggested co-localization of FS and FA associated break-points (FA-bp) was studied here for the first time systematically by molecular cytogenetics. Metaphase chromosomes were obtained from lymphocytes of two FA patients (FANC-A and FANC-C, respectively). Overall 50.58% of the investigated FA-bp correspond to cytogenetic regions with kno...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136092</comments>
            <pubDate>Sat, 02 Jan 2010 08:49:14 +0100</pubDate>
            <guid isPermaLink="false">3136092</guid>        </item>
        <item>
            <title>Talaporfin-mediated photodynamic therapy for peritoneal metastasis of gastric cancer in an in vivo mouse model: drug distribution and efficacy studies.</title>
            <link>http://www.medworm.com/index.php?rid=3136091&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%3D20043064%26dopt%3DAbstract</link>
            <description>We examined the accumulation of talaporfin in peritoneal metastatic nodules and determined the optimal laser condition for these nodules. We also evaluated the pathological response after therapy. We created a peritoneal metastasis model in nude mice using the MKN-45 EGFP cell line. We evaluated the accumulation of talaporfin in peritoneal metastatic nodules and normal organs by spectrophotometric analysis 2-8 h after i.p. talaporfin. To determine optimal PDT conditions, we treated metastatic nodules and the small intestine using multiple laser doses (2, 5, and 10 J/cm2, respectively). Accumulation of talaporfin was detected in metastatic nodules in higher intensities than in the small intestine. The fluorescent intensity of the peritoneal metastatic nodules gradually decreased dependent o...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136091</comments>
            <pubDate>Sat, 02 Jan 2010 08:49:11 +0100</pubDate>
            <guid isPermaLink="false">3136091</guid>        </item>
        <item>
            <title>Forkhead box A1 transcriptional pathway in KRT7-expressing esophageal squamous cell carcinomas with extensive lymph node metastasis.</title>
            <link>http://www.medworm.com/index.php?rid=3136090&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%3D20043065%26dopt%3DAbstract</link>
            <description>Authors: Sano M, Aoyagi K, Takahashi H, Kawamura T, Mabuchi T, Igaki H, Tachimori Y, Kato H, Ochiai A, Honda H, Nimura Y, Nagino M, Yoshida T, Sasaki H
    Prognosis of cancers with lymph node metastasis is known to be very poor; however, it is still controversial whether metastatic potential can be evaluated by expression profiles of primary tumors. Therefore, to address this issue, we compared gene expression profiles of 24 esophageal squamous cell carcinomas (ESCCs) with extensive lymph node metastasis and 11 ESCCs with no metastatic lymph node. However, there was no gene cluster distinguishing these two groups, suggesting that lymph node metastasis-associated genes are varied depending on cases or subgroups. Therefore, we applied a recently developed filtering method (S2N') to identify...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136090</comments>
            <pubDate>Sat, 02 Jan 2010 08:49:06 +0100</pubDate>
            <guid isPermaLink="false">3136090</guid>        </item>
        <item>
            <title>Expression of fibroblast growth factor receptor 2 IIIc in human uterine cervical intraepithelial neoplasia and cervical cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3136089&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%3D20043066%26dopt%3DAbstract</link>
            <description>In this study, we determined the expression and roles of FGFR2 IIIc in cervical intraepithelial neoplasia (CIN) and cervical cancer. In CINs 1 and 2, FGFR2 IIIc was found to be localized at the basal to lower two-thirds of the squamous epithelium, whereas it was localized in most of the squamous epithelium, except for the superficial layer in CIN 3. In situ hybridization (ISH) analysis showed that the expression patterns of FGFR2 IIIc mRNA are similar to those of FGFR2 IIIc protein in CINs. The FGFR2 IIIc protein was detected in all invasive cervical cancer patients (29 cases) and its mRNA was found to be strongly expressed in the invasive front of cancer cell nests. FGFR2 IIIc cDNA was stably transfected into CaSki cells, which are derived from a cervical SCC. The growth rates of the CaSk...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136089</comments>
            <pubDate>Sat, 02 Jan 2010 08:49:03 +0100</pubDate>
            <guid isPermaLink="false">3136089</guid>        </item>
        <item>
            <title>Tranilast strongly sensitizes pancreatic cancer cells to gemcitabine via decreasing protein expression of ribonucleotide reductase 1.</title>
            <link>http://www.medworm.com/index.php?rid=3136088&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%3D20043067%26dopt%3DAbstract</link>
            <description>Authors: Mitsuno M, Kitajima Y, Ohtaka K, Kai K, Hashiguchi K, Nakamura J, Hiraki M, Noshiro H, Miyazaki K
    Gemcitabine (Gem) is a dFdC analogue with activity against several solid tumors. Gem is intracellularly phosphorylated by dCK, leading to the production of the metabolite dFdCDP. dFdCDP exhibits the cytotoxic effect by inactivating ribonucleotide reductase larger subunit 1 (RRM1), which is a rate limiting enzyme for de novo DNA synthesis. To date, RRM1 expression is believed to determine sensitivity to Gem in pancreatic and non-small cell lung cancer. In the present study, we found that an anti-allergic drug, tranilast strongly enhanced the sensitivity of pancreatic cancer cell line KP4 to Gem. In growth inhibition assay, 100 microM of tranilast plus 1 microM of Gem more strongly ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136088</comments>
            <pubDate>Sat, 02 Jan 2010 08:49:01 +0100</pubDate>
            <guid isPermaLink="false">3136088</guid>        </item>
        <item>
            <title>Expression of dipeptidyl peptidase-IV activity and/or structure homologs in human meningiomas.</title>
            <link>http://www.medworm.com/index.php?rid=3136087&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%3D20043068%26dopt%3DAbstract</link>
            <description>In this study, we investigated 22 human meningiomas for the expression of dipeptidyl peptidase (DPP)-IV activity and/or structure homologs (DASH), including canonical DPP-IV/CD26, fibroblast activation protein-alpha (FAPalpha), DPP8 and DPP9. DPP-IV-like enzymatic activity, including all enzymatically-active DASH molecules, was found in all 18 benign meningiomas WHO grade I and IV atypical meningiomas WHO grade II by continuous rate fluorimetric assay in tissue homogenates and catalytic enzyme histochemistry in situ. In atypical meningiomas, this activity was significantly higher and was associated with higher cell proliferation as detected by Ki67 antigen immunohistochemistry. The expression of DPP-IV/CD26 and FAPalpha demonstrated by real-time RT-PCR and immunohistochemistry was low. As ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136087</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:58 +0100</pubDate>
            <guid isPermaLink="false">3136087</guid>        </item>
        <item>
            <title>Silencing the Peroxiredoxin III gene inhibits cell proliferation in breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3136086&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%3D20043069%26dopt%3DAbstract</link>
            <description>In this study, we evaluated the expression of Prx III in breast cancer tissues and elucidated its role in cell proliferation, a hallmark of cancer. Breast tissue microarrays comprising 106 breast cancer sections were stained with Prx III antibody using immunohistochemisty and correlated with proliferating cell nuclear antigen (PCNA) immunostaining. To validate the role of Prx III in cell proliferation, expression of Prx III was analyzed at the mRNA and protein levels by real-time RT-PCR, Western blotting and immunofluorescence in vitro. siRNA mediated silencing of Prx III in MDA-MB-231 breast cancer cells was performed and the effect on the cell cycle was examined. Prx III expression in patient tissue microarray samples was found to be positively associated with PCNA immunostaining, a prol...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136086</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:55 +0100</pubDate>
            <guid isPermaLink="false">3136086</guid>        </item>
        <item>
            <title>Immunotherapy of breast cancer by single delivery with rAAV2-mediated interleukin-15 expression.</title>
            <link>http://www.medworm.com/index.php?rid=3136085&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%3D20043070%26dopt%3DAbstract</link>
            <description>In this study, the rAAV2-hIL15 vector was produced and subjected for treatment with xenograft JC breast cancer model. Results showed that tumor onset was significantly delayed, the tumor growth was suppressed, and the lifespan of tumor-bearing mice were prolonged by rAAV2-hIL15. In addition, rAAV2-hIL15 was able to produce a substantial expression of IL15 protein that ultimately activated the cytotoxic activity of LAK cells. Furthermore, prominent apoptosis was observed in tumor lesions following injection of rAAV2-hIL15. Taken together, our results suggested that rAAV2-hIL15 appears as a new potential therapeutic tool for breast cancer immunotherapy.
    PMID: 20043070 [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=3136085</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:53 +0100</pubDate>
            <guid isPermaLink="false">3136085</guid>        </item>
        <item>
            <title>Combined external and intracavitary irradiation in treatment of advanced cervical carcinomas: predictive factors for local tumor control and early recurrences.</title>
            <link>http://www.medworm.com/index.php?rid=3136084&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%3D20043071%26dopt%3DAbstract</link>
            <description>Authors: Sorbe B, Bohr L, Karlsson L, Bermark B
    In a series of 131 primary cervical carcinomas in FIGO stages I-IV suitable for combined external pelvic and intraluminal cervical-vaginal brachytherapy predictive and prognostic factors were analyzed with regard to locoregional tumor control, recurrences and survival data. Patients with prior surgery or patients treated with external beam therapy alone were excluded from this series. Concomitant chemotherapy was given to 47 patients (36%). The external beam therapy was given with a four-field technique (50-60 Gy) and brachytherapy with high dose-rate (Ir-192) using a ring applicator set. The dose (18-30 Gy) was specified according to the rules in ICRU 38 (a minimum dose to the surface of the target volume). Three or five fractions were g...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136084</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:50 +0100</pubDate>
            <guid isPermaLink="false">3136084</guid>        </item>
        <item>
            <title>Rho GDP dissociation inhibitor alpha expression correlates with the outcome of CMF treatment in invasive ductal breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3136083&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%3D20043072%26dopt%3DAbstract</link>
            <description>Authors: Ronneburg H, Span PN, Kantelhardt E, Dittmer A, Schunke D, Holzhausen HJ, Sweep FC, Dittmer J
    Rho-GDIalpha is an inhibitor of Rho-GTPases, which is involved in cancer progression. Little is known about its role in breast cancer progression. There is evidence, that Rho-GDIalpha may modulate drug resistance of breast cancer cells. To assess the importance of Rho-GDIalpha as a risk factor in invasive ductal breast cancer, cancer specimens of three groups of patients were analyzed for Rho-GDIalpha RNA (group 1, N=72 and group 2, N=73) or protein expression (group 3, N=90). In group 1, patients did not receive any adjuvant treatment, whereas, in groups 2 and 3, patients were treated with anti-estrogens and/or with chemotherapeutical drugs. Rho-GDIalpha RNA levels, measured by RT-PC...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136083</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:47 +0100</pubDate>
            <guid isPermaLink="false">3136083</guid>        </item>
        <item>
            <title>Implication of PI3K-dependent HSP27 and p53 expression in mild heat shock-triggered switch of metabolic stress-induced necrosis to apoptosis in A549 cells.</title>
            <link>http://www.medworm.com/index.php?rid=3136082&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%3D20043073%26dopt%3DAbstract</link>
            <description>In conclusion, these results indicate that PI3K-dependent HSP27 and p53 induction and PI3K- and ERK1/2-dependent inhibition of the GD-induced increase in RIPA-insoluble HSP27 and p53 protein levels by heat play a key role(s) in heat shock-mediated switch of GD-induced necrosis to apoptosis.
    PMID: 20043073 [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=3136082</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:45 +0100</pubDate>
            <guid isPermaLink="false">3136082</guid>        </item>
        <item>
            <title>Cytotoxic effects of ultra-diluted remedies on breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3136081&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%3D20043074%26dopt%3DAbstract</link>
            <description>Authors: Frenkel M, Mishra BM, Sen S, Yang P, Pawlus A, Vence L, Leblanc A, Cohen L, Banerji P, Banerji P
    The use of ultra-diluted natural products in the management of disease and treatment of cancer has generated a lot of interest and controversy. We conducted an in vitro study to determine if products prescribed by a clinic in India have any effect on breast cancer cell lines. We studied four ultra-diluted remedies (Carcinosin, Phytolacca, Conium and Thuja) against two human breast adenocarcinoma cell lines (MCF-7 and MDA-MB-231) and a cell line derived from immortalized normal human mammary epithelial cells (HMLE). The remedies exerted preferential cytotoxic effects against the two breast cancer cell lines, causing cell cycle delay/arrest and apoptosis. These effects were accompani...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136081</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:42 +0100</pubDate>
            <guid isPermaLink="false">3136081</guid>        </item>
        <item>
            <title>An 8-gene signature, including methylated and down-regulated glutathione peroxidase 3, of gastric cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3136080&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%3D20043075%26dopt%3DAbstract</link>
            <description>Authors: Zhang X, Yang JJ, Kim YS, Kim KY, Ahn WS, Yang S
    We have identified an 8-gene signature with significant expression differences between gastric cancer and normal gastric tissues. This 8-gene set can predict the normal and cancer status of gastric tissues with more than 96% accuracy in a totally independent microarray dataset. The 8 genes are composed of down-regulated KLF4, GPX3, SST and LIPF, together with up-regulated SERPINH1, THY1 and INHBA in gastric cancer. To corroborate the differential gene expression pattern, we chose GPX3 and examined its expression pattern in detail. A comparison of GPX3 expression pattern shows a broader down-regulated pattern in multiple types of cancers, including cervical, thyroid, head and neck, lung cancers and melanoma than in healthy contro...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136080</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:39 +0100</pubDate>
            <guid isPermaLink="false">3136080</guid>        </item>
        <item>
            <title>Integrative genomic analyses of CXCR4: transcriptional regulation of CXCR4 based on TGFbeta, Nodal, Activin signaling and POU5F1, FOXA2, FOXC2, FOXH1, SOX17, and GFI1 transcription factors.</title>
            <link>http://www.medworm.com/index.php?rid=3136079&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%3D20043076%26dopt%3DAbstract</link>
            <description>Authors: Katoh M, Katoh M
    CXCR4, CD133, CD44 and ABCG2 are representative transmembrane proteins expressed on the surfaces of normal and/or cancer stem cells. CXCR4 is co-expressed with POU5F1 in endodermal precursors and adult-tissue stem cells. CXCR4 is expressed in a variety of human tumors, such as breast cancer, prostate cancer, pancreatic cancer, and gastric cancer. CXCR4 is a G protein-coupled receptor (GPCR) for CXCL12 (SDF1) chemokine, and the CXCL12-CXCR4 signaling axis is involved in proliferation, survival, migration, and homing of cancer cells. Integrative genomic analyses of CXCR4 gene were carried out to elucidate the mechanisms of CXCR4 expression in stem cells, because CXCR4 is a key molecule occupying the crossroads of oncology, immunology, gerontology and regenerativ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136079</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:36 +0100</pubDate>
            <guid isPermaLink="false">3136079</guid>        </item>
        <item>
            <title>Punicic acid is an omega-5 fatty acid capable of inhibiting breast cancer proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=3136078&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%3D20043077%26dopt%3DAbstract</link>
            <description>Authors: Grossmann ME, Mizuno NK, Schuster T, Cleary MP
    Pomegranate extracts have been used as anticancer agents and they contain a large number of potentially bioactive substances. Punicic acid is an omega-5 long chain polyunsaturated fatty acid found in Punica granatum (pomegranate) seed oil. A number of long chain fatty acids have been reported to have cancer preventive actions. Here we investigated the potential ability of punicic acid to affect growth of both an estrogen insensitive breast cancer cell line (MDA-MB-231) and an estrogen sensitive cell line developed from the MDA-MB-231 cells (MDA-ERalpha7). Proliferation was inhibited 92 and 96% for MDA-MB-231 and MDA-ERalpha7 cells, respectively compared to untreated cells by 40 microM punicic acid. Furthermore, punicic acid induce...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136078</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:34 +0100</pubDate>
            <guid isPermaLink="false">3136078</guid>        </item>
        <item>
            <title>A kelch family protein Nd1-L functions as a metastasis suppressor in cancer cells via Rho family proteins mediated mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=3136077&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%3D20043078%26dopt%3DAbstract</link>
            <description>We examined the effect of Nd1-L on cancer cell invasion and metastasis. Over-expression of Nd1-L in murine colon carcinoma cell line Colon 26 and murine melanoma cell line B16 resulted in suppression of pulmonary and liver metastasis after inoculation of these cells to syngeneric mice and in increased survival in an animal model. On the other hand, knock down of Nd1-L by RNA interference promoted metastasis ability of these cells. Increased expression of Nd1-L inhibited migration and Matrigel invasion capacity of cancer cell lines in vitro. Thus, Nd1-L expression inversely correlated with invasive and metastasis capacity of cancer cells. Furthermore, increased expression of Nd1-L in NIH3T3 cells inhibited growth factor induced activation of Rho family small GTPases such as Rho, Rac and cdc...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136077</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:31 +0100</pubDate>
            <guid isPermaLink="false">3136077</guid>        </item>
        <item>
            <title>Xanthohumol, a prenylated chalcone derived from hops, inhibits proliferation, migration and interleukin-8 expression of hepatocellular carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3136076&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%3D20043079%26dopt%3DAbstract</link>
            <description>Authors: Dorn C, Weiss TS, Heilmann J, Hellerbrand C
    Xanthohumol, the major prenylated chalcone found in hops, is well known to exert anti-cancer effects, but information regarding the impact on hepatocellular carcinoma (HCC) cells and potential adverse effects on non-tumorous hepatocytes is limited. Here, we show that xanthohumol at a concentration of 25 microM induced apoptosis in two HCC cell lines (HepG2 and Huh7). Furthermore, xanthohumol repressed proliferation and migration, as well as TNF induced NF-kappaB activity and interleukin-8 expression in both cell lines at even lower concentrations. In contrast, xanthohumol concentrations up to 100 microM did not affect viability of primary human hepatocytes in vitro. In summary, our data showed that xanthohumol can ameliorate differen...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136076</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:29 +0100</pubDate>
            <guid isPermaLink="false">3136076</guid>        </item>
        <item>
            <title>Androgen regulated TRPM8 expression: a potential mRNA marker for metastatic prostate cancer detection in body fluids.</title>
            <link>http://www.medworm.com/index.php?rid=3136075&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%3D20043080%26dopt%3DAbstract</link>
            <description>Authors: Bai VU, Murthy S, Chinnakannu K, Muhletaler F, Tejwani S, Barrack ER, Kim SH, Menon M, Veer Reddy GP
    Identification of sensitive and specific biomarkers for early detection and prognosis of prostate cancer is essential for timely and appropriate treatment of the disease in individual patients. We identified an RNA transcript with sequence homology to TRPM8 (melastatin-related transient receptor potential member 8) that was overexpressed in tumor vs. patient-matched non-tumor prostate tissues by RT-PCR differential display (DD). Semi-quantitative RT-PCR analysis revealed that TRPM8 levels were higher in tumor than in non-tumor tissue from 31 of 40 (&amp;gt;75%) patients examined. Overexpression of TRPM8 was independent of changes in androgen receptor (AR) mRNA levels in tumor tissu...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136075</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:26 +0100</pubDate>
            <guid isPermaLink="false">3136075</guid>        </item>
        <item>
            <title>Expression of estrogen receptor alpha with a Tet-off adenoviral system induces G0/G1 cell cycle arrest in SKBr3 breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3136074&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%3D20043081%26dopt%3DAbstract</link>
            <description>In this study, we have built on previous studies by developing a Tet-off adenoviral system to express ERalpha in the ER-negative SKBr3 breast cancer cells that over-express both EGFR and HER2. This system efficiently delivers ERalpha and the expression level of ERalpha is controlled by doxycycline in a concentration-dependent manner. The growth of SKBr3 was inhibited by ERalpha expression and further inhibited in the presence of 1 nM 17beta-estradiol. SKBr3 cells were arrested at G0/G1 cell cycle upon ERalpha expression, which corresponded to an increase of p21Cip1/Waf1, hypo-phosphorylation of pRb and decrease of E2F1. Estrogen also reduced EGFR and HER2 expression in SKBr3 cells after ERalpha was expressed. Given that estrogen-induced increase of p21Cip1/Waf1 and decrease of E2F1 was als...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136074</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:23 +0100</pubDate>
            <guid isPermaLink="false">3136074</guid>        </item>
        <item>
            <title>Regulation of heat shock protein 70-1 expression by androgen receptor and its signaling in human prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=3136073&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%3D20043082%26dopt%3DAbstract</link>
            <description>Authors: Lu S, Tan Z, Wortman M, Lu S, Dong Z
    Heat shock protein (hsp) 70-1 (hsp70-1) is overexpressed in human prostate cancer cells and may play important roles in prostate cancer resistance to conventional therapies. The purpose of this study was to investigate whether androgen receptor (AR) and its signaling regulate hsp70-1 expression. Several lines of AR-positive (LNCaP, LAPC-4, and 22Rv1) and -negative (PC-3, DU145, WPE1-NB14 and WPE1-NB-26) human prostatic cells were used in the study. Dihydrotestosterone (DHT) enhanced hsp70-1 expression in LNCaP cells. Expression of hsp70-1 in LNCaP cells was downregulated by the anti-androgens bicalutamide (Bic), and flutamide (Flut), and a newly identified AR signaling antagonist DL3. The downregulation of hsp70-1 by DL3 was also observed i...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136073</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:19 +0100</pubDate>
            <guid isPermaLink="false">3136073</guid>        </item>
        <item>
            <title>Receptor and enzyme expression for prostanoid metabolism in colorectal cancer related to tumor tissue PGE2.</title>
            <link>http://www.medworm.com/index.php?rid=3136072&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%3D20043083%26dopt%3DAbstract</link>
            <description>Authors: Gustafsson A, Andersson M, Lagerstedt K, L&amp;#xF6;nnroth C, Nordgren S, Lundholm K
    Prostaglandins support progression of colorectal cancer by several mechanisms. This conclusion is based on epidemiological and drug intervention long-term studies or retrieved from animal and cell culture experiments. The aim of the present study was to map receptor and enzyme expression for prostanoid metabolism in the presence of high or low PGE2 content within colon cancer tissue at primary tumor operation and after short-term preoperative provision of non-steroidal anti-inflammatory drug (NSAID). Twenty-three unselected patients with colon cancer were randomly selected to receive indomethacin (NSAID) or sham treatment for 3 days before surgery. Normal colon and tumor tissue were collected at o...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136072</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:16 +0100</pubDate>
            <guid isPermaLink="false">3136072</guid>        </item>
        <item>
            <title>FBXL16 is a novel E2F1-regulated gene commonly upregulated in p16INK4A- and p14ARF-silenced HeLa cells.</title>
            <link>http://www.medworm.com/index.php?rid=3136071&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%3D20043084%26dopt%3DAbstract</link>
            <description>Authors: Sato K, Kusama Y, Tategu M, Yoshida K
    Two crucial cell cycle regulators, p16INK4A and p14ARF, are produced from the cyclin-dependent kinase inhibitor 2A (CDKN2A) gene locus by alternative reading frames; these regulators act as tumor suppressors during tumorigenesis. However, the molecular events incidental to the acute functional loss of CDKN2A remain a critical issue. Two pivotal regulatory pathways of cell fate determination involving p16INK4A/retinoblastoma protein (pRb)/E2F1 and p14ARF/p53 interact tightly with each other; however, novel factors with an integral or overlapping role in these two pathways remain incompletely defined. To this end, we specifically decreased the expression of p16INK4A or p14ARF proteins using RNA interference (RNAi) in HeLa cells. Using a DNA ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136071</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:14 +0100</pubDate>
            <guid isPermaLink="false">3136071</guid>        </item>
        <item>
            <title>Inhibition of glutathione-S-transferase as a treatment strategy for multidrug resistance in childhood rhabdomyosarcoma.</title>
            <link>http://www.medworm.com/index.php?rid=3136070&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%3D20043085%26dopt%3DAbstract</link>
            <description>Authors: Seitz G, Bonin M, Fuchs J, Poths S, Ruck P, Warmann SW, Armeanu-Ebinger S
    Multidrug resistance (MDR) is a common problem in the treatment of childhood rhabdomyosarcoma (RMS). A complete reversal of MDR is currently not possible. The aim of this study was to investigate the role of glutathione-S-transferase (GST) as mechanism of MDR in childhood RMS and to analyze possible reversal strategies. Female athymic mice underwent xenotransplantation with embryonal or alveolar RMS cells and were treated with vincristine. Gene expression analysis using Affymetrix HU-Gene 1.0 arrays revealed 2314 differentially expressed genes between the groups in alveolar RMS and 1387 in embryonal RMS. Ingenuity pathway analysis revealed a cluster of 5 overexpressed genes of the GST family in animals t...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136070</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:11 +0100</pubDate>
            <guid isPermaLink="false">3136070</guid>        </item>
        <item>
            <title>ErbB2-enhanced invasiveness of H-Ras MCF10A breast cells requires MMP-13 and uPA upregulation via p38 MAPK signaling.</title>
            <link>http://www.medworm.com/index.php?rid=3136069&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%3D20043086%26dopt%3DAbstract</link>
            <description>Authors: Yong HY, Kim IY, Kim JS, Moon A
    Overexpression of ErbB2 has been frequently found in mammary carcinoma. We have previously shown that the aberrant activation of H-Ras induces human breast cell invasion and migration. The present study was aimed at investigating the effect of ErbB2 overexpression on H-Ras-induced breast cell invasion and to elucidate the underlying mechanisms. Herein, we show that overexpression of ErbB2 promotes invasive and migratory abilities of H-Ras-activated MCF10A human breast epithelial cells through upregulation of matrix metalloproteinase (MMP)-13 and urokinase-type plasminogen activator (uPA). We also demonstrate that the p38 MAPK is an important signaling molecule in the ErbB2-induced upregulation of MMP-13 and uPA and invasion/migration of H-Ras MC...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136069</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:08 +0100</pubDate>
            <guid isPermaLink="false">3136069</guid>        </item>
        <item>
            <title>Overexpression of Cdx2 inhibits progression of gastric cancer in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=3136068&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%3D20043087%26dopt%3DAbstract</link>
            <description>Authors: Xie Y, Li L, Wang X, Qin Y, Qian Q, Yuan X, Xiao Q
    The caudal-type homeobox gene Cdx2 encodes a transcription factor which in adult mammals is expressed in the cells of the intestinal epithelium and is thought to play an important role in their proliferation and differentiation. Cdx2 mediates apoptosis and suppresses tumorigenesis in many tissue types, but there are few data available on Cdx2 expression and its relationship to tumor kinetics in gastric cancer. To gain better insight into the involvement of Cdx2 in the biological characteristics of gastric cancer, we investigated the effect of Cdx2 overexpression on the progression of gastric carcinoma cells. A gastric cancer cell line stably overexpressing Cdx2 (MGC-803/Cdx2) was established. The influence of Cdx2 overexpressi...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3136068</comments>
            <pubDate>Sat, 02 Jan 2010 08:48:06 +0100</pubDate>
            <guid isPermaLink="false">3136068</guid>        </item>
        <item>
            <title>Angiogenesis: An update and potential drug approaches (Review).</title>
            <link>http://www.medworm.com/index.php?rid=3057624&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%3D19956828%26dopt%3DAbstract</link>
            <description>This report will review some of the recent developments and most significant advances in this field and outline future challenges and directions.
    PMID: 19956828 [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=3057624</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:26 +0100</pubDate>
            <guid isPermaLink="false">3057624</guid>        </item>
        <item>
            <title>A novel pharmacodynamic approach to assess and predict tumor response to the epidermal growth factor receptor inhibitor gefitinib in patients with esophageal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3057623&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%3D19956829%26dopt%3DAbstract</link>
            <description>This study aimed to describe a short-term ex vivo assay to predict response to epidermal growth factor receptor (EGFR) targeted therapy (gefitinib) in adenocarcinoma patients. Four patients with locally advanced esophageal adenocarcinoma were treated with gefitinib (250 mg/day) for 14 days and pharmacokinetic (PK) studies were conducted to monitor plasma drug concentrations. Tumor cells were sampled by endoscopic biopsy prior to (baseline, day 0) and at the completion of (day 14) treatment. Cells obtained at baseline were exposed to gefitinib in short-term cell culture conditions (ex vivo assay). Western blot analyses with phospho-specific antibodies were performed to evaluate activation and biochemical response to therapy of EGFR and its downstream signaling components ERK and AKT ex vivo...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057623</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:23 +0100</pubDate>
            <guid isPermaLink="false">3057623</guid>        </item>
        <item>
            <title>PNA-mediated modulation and redirection of Her-2 pre-mRNA splicing: Specific skipping of erbB-2 exon 19 coding for the ATP catalytic domain.</title>
            <link>http://www.medworm.com/index.php?rid=3057622&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%3D19956830%26dopt%3DAbstract</link>
            <description>Authors: Pankratova S, Nielsen BN, Shiraishi T, Nielsen PE
    The Her-2 receptor coded for by the proto-oncogenic erbB-2 gene is a clinically validated target for treatment of a significant genetic subclass of breast cancers, and Her-2 is also overexpressed or mutated in a range of other cancers. In an approach to exploit antisense mediated splicing interference as a means of manipulating erbB-2 expression in a therapeutically relevant fashion, we have studied the effect on mRNA splicing of a series of peptide nucleic acid (PNA) oligomers targeting specific intron-exon junctions in the erbB-2 pre-mRNA. In particular, we are interested in identifying PNA oligomers that specifically induce skipping of exon 19 as this exon is coding for the ATP catalytic domain of Her-2, and if expressed suc...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057622</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:20 +0100</pubDate>
            <guid isPermaLink="false">3057622</guid>        </item>
        <item>
            <title>Cyclin D1b represses breast cancer cell growth by antagonizing the action of cyclin D1a on estrogen receptor alpha-mediated transcription.</title>
            <link>http://www.medworm.com/index.php?rid=3057621&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%3D19956831%26dopt%3DAbstract</link>
            <description>In this study, we determined that cyclin D1b is incapable of inducing ERalpha-mediated transcription because it fails to recruit steroid receptor coactivator-1 (SRC-1) to ERalpha. Moreover, cyclin D1b antagonizes cyclin D1a-induced ERalpha-mediated transcription by competing with cyclin D1a for ERalpha binding. Cell proliferation assay showed that cyclin D1b repressed the ERalpha-positive breast cancer T47D cell growth. Our findings suggest that the cyclin D1b represses breast cancer cell growth by antagonizing the action of cyclin D1a on ERalpha-mediated transcription.
    PMID: 19956831 [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=3057621</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:16 +0100</pubDate>
            <guid isPermaLink="false">3057621</guid>        </item>
        <item>
            <title>Active Wnt signalling is associated with low differentiation and high proliferation in human biliary tract cancer in vitro and in vivo and is sensitive to pharmacological inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=3057620&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%3D19956832%26dopt%3DAbstract</link>
            <description>Authors: Kiesslich T, Alinger B, Wolkersd&amp;#xF6;rfer GW, Ocker M, Neureiter D, Berr F
    Activation of developmental pathways has been recognized as a key mechanism for tumourigenesis and, hence, might be a valuable target for otherwise difficult to treat tumour entities such as biliary tract cancer (BTC). Therefore, we performed a comprehensive analysis of the Wnt signalling pathway in 9 BTC cell lines on cell blocks, xenograft tumours and on human tissue microarrays by real-time reverse transcription PCR and by immunochemistry. Furthermore, the effects of pharmacological pathway inhibition were investigated. As a result we found a significant positive correlation of Wnt pathway activation with cyclin D1 expression and the proliferation parameters Ki67, cell cycle distribution, and growth...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057620</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:13 +0100</pubDate>
            <guid isPermaLink="false">3057620</guid>        </item>
        <item>
            <title>Inhibition of AP-1 and MAPK signaling and activation of Nrf2/ARE pathway by quercitrin.</title>
            <link>http://www.medworm.com/index.php?rid=3057619&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%3D19956833%26dopt%3DAbstract</link>
            <description>Authors: Ding M, Zhao J, Bowman L, Lu Y, Shi X
    Quercitrin, glycosylated form of flavonoid compounds, is widely distributed in nature. Extensive studies have demonstrated that quercitrin exhibits strong antioxidant and anti-carcinogenic activities. However, the molecular mechanism is poorly understood. The present study examines the effects of quercitrin on tumor promotion in mouse JB6 cells, a validated model for screening cancer chemopreventive agents and elucidating the molecular mechanisms. Quercitrin blocked TPA-induced neoplastic transformation in JB6 P+ cells. Pretreatment of JB6 cells with quercitrin down-regulated transactivation of AP-1 and NF-kappaB induced by UVB or TPA. In the skin of AP-1-luciferase transgenic mice, topical treatment of the mouse with quercitrin markedly b...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057619</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:11 +0100</pubDate>
            <guid isPermaLink="false">3057619</guid>        </item>
        <item>
            <title>Atelocollagen-delivered siRNA targeting the FABP5 gene as an experimental therapy for prostate cancer in mouse xenografts.</title>
            <link>http://www.medworm.com/index.php?rid=3057618&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%3D19956834%26dopt%3DAbstract</link>
            <description>Authors: Forootan SS, Bao ZZ, Forootan FS, Kamalian L, Zhang Y, Bee A, Foster CS, Ke Y
    The gene FABP5 encodes cutaneous fatty acid binding protein (C-FABP) that is up-regulated in prostate cancer where it acts as a putative oncogene. To test the hypothesis that siRNA to FABP5 delivered to the external environment of a prostate cancer would reduce the level of C-FABP in vivo, experiments were established whereby siRNA to FABP5 suspended in atelocollagen was injected around tumour masses produced by PC-3M cells in Balb/c nude mice and compared with the effect of non-specific scrambled siRNA in atelocollagen. At autopsy, the average size of tumours from the groups treated with 10 and 15 microM siRNA in atelocollagen was significantly (p=0.02) reduced by more than 3-fold, when compared to ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057618</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:08 +0100</pubDate>
            <guid isPermaLink="false">3057618</guid>        </item>
        <item>
            <title>Target chemotherapy of anti-CD147 antibody-labeled liposome encapsulated GSH-DXR conjugate on CD147 highly expressed carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3057617&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%3D19956835%26dopt%3DAbstract</link>
            <description>Authors: Matsudaira H, Asakura T, Aoki K, Searashi Y, Matsuura T, Nakajima H, Tajiri H, Ohkawa K
    It was confirmed that CD147 (Emmprin) was expressed on the cell surface of carcinoma cells. For the purpose of studying the efficacy of a CD147-targeting agent on CD147-expressing carcinoma cells, we investigated the effect of a conjugate of glutathione-doxorubicin (GSH-DXR) encapsulated in an anti-CD147 antibody-labeled liposome (aCD147ab-liposome) in terms of specific accumulation and cytotoxicity in CD147-expressing human carcinoma cells. Expression of CD147 was not observed in many normal human tissues. However, slight expression of CD147 in kidney, prostate and breast tissues was observed. By contrast, high-level expression of CD147 in all carcinoma cells such as A431, PC3 and Ishikawa...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057617</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:05 +0100</pubDate>
            <guid isPermaLink="false">3057617</guid>        </item>
        <item>
            <title>Epigenetic silencing of RELN in gastric cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3057616&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%3D19956836%26dopt%3DAbstract</link>
            <description>Authors: Dohi O, Takada H, Wakabayashi N, Yasui K, Sakakura C, Mitsufuji S, Naito Y, Taniwaki M, Yoshikawa T
    RELN (Reelin) is an extracellular glycoprotein that plays a critical role in neuronal migration. Here we show that the RELN gene is frequently silenced in gastric cancers (GCs) by aberrant promoter hypermethylation. Although RELN was strongly expressed in non-tumor gastric epithelia, its expression was weak, or absent, in GC cell lines and primary GC tumors. Absence of RELN expression significantly correlated with a more advanced stage of GC. Methylation of the RELN promoter was frequently found in GC cell lines and in primary GC tumors. These findings suggest that disruption of the RELN pathway may be involved in gastric carcinogenesis.
    PMID: 19956836 [PubMed - in process] ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057616</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:03 +0100</pubDate>
            <guid isPermaLink="false">3057616</guid>        </item>
        <item>
            <title>Differential proteomic analysis of hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3057615&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%3D19956837%26dopt%3DAbstract</link>
            <description>Authors: Corona G, De Lorenzo E, Elia C, Simula MP, Avellini C, Baccarani U, Lupo F, Tiribelli C, Colombatti A, Toffoli G
    The principal aim of the present study consisted in the identification of the disregulated proteins associated with the development of hepatocellular carcinoma (HCC). The differences in protein expression between hepatocellular carcinoma (HCC) and the corresponding non-HCC liver tissues were investigated in a cohort of 20 patients using two-dimensional fluorescence difference in gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS). The up- and down-regulated protein spots that exhibited 1.5-fold difference signal intensity with statistical significance (p&amp;lt;0.05, t-test, confidence intervals 95%) were excised from the gel and identified by peptide mass...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057615</comments>
            <pubDate>Sat, 05 Dec 2009 13:33:00 +0100</pubDate>
            <guid isPermaLink="false">3057615</guid>        </item>
        <item>
            <title>Use of protein array to investigate receptor tyrosine kinases activated in gastric cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3057614&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%3D19956838%26dopt%3DAbstract</link>
            <description>Authors: Gong J, Morishita A, Kurokohchi K, Tani J, Kato K, Miyoshi H, Inoue H, Kobayashi M, Liu S, Murota M, Muramatsu A, Izuishi K, Suzuki Y, Yoshida H, Uchida N, Deguchi K, Iwama H, Ishimaru I, Masaki T
    Our study used protein array technology to analyze the expression status of various activated receptor tyrosine kinases (RTKs) in gastric carcinoma; then, we sought to discover an effective therapeutic receptor tyrosine kinase for this disease and investigated the anti-tumor mechanism of the therapeutic RTK. In addition to the expressions of activated RTKs in human gastric cancer and adjacent normal mucosa, the expression of activated RTKs in gastric cancer cell lines, MKN74, MKN45, MKN7 and MKN1, were also studied. The RTKs activated in gastric cancer tissue are EGFR, ErbB2, FGFR1, ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057614</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:57 +0100</pubDate>
            <guid isPermaLink="false">3057614</guid>        </item>
        <item>
            <title>Serine 2481-autophosphorylation of mammalian target of rapamycin (mTOR) couples with chromosome condensation and segregation during mitosis: Confocal microscopy characterization and immunohistochemical validation of PP-mTORSer2481 as a novel high-contrast mitosis marker in breast cancer core biopsies.</title>
            <link>http://www.medworm.com/index.php?rid=3057613&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%3D19956839%26dopt%3DAbstract</link>
            <description>Authors: Lopez-Bonet E, Vazquez-Martin A, P&amp;#xE9;rez-Mart&amp;#xED;nez MC, Oliveras-Ferraros C, P&amp;#xE9;rez-Bueno F, Bernad&amp;#xF3; L, Menendez JA
    The prognostic abilities of breast cancer gene expression signatures are due mostly to the detection of proliferation activity. One of the strongest, yet simple and well-reproducible proliferation-associated prognostic factors is the mitotic activity index (MAI). However: a) counting mitotic figures is regarded by many histopathologists as cumbersome and time-consuming, and b) most available immunohistochemical markers are much weaker predictors than the MAI. We have investigated the spatio-temporal sub-cellular distribution of the Serine 2481-autophosphorylated form of mTOR (PP-mTORSer2481) during the G1/S-to-M-phase transition both in cultured ca...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057613</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:55 +0100</pubDate>
            <guid isPermaLink="false">3057613</guid>        </item>
        <item>
            <title>Hypoxia switches glucose depletion-induced necrosis to phosphoinositide 3-kinase/Akt-dependent apoptosis in A549 lung adenocarcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3057612&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%3D19956840%26dopt%3DAbstract</link>
            <description>In conclusion, our results demonstrate that hypoxia switches GD-induced necrosis to apoptosis and ERK1/2 and PI3K-Akt exert anti-necrotic and pro-apoptotic activities in the cell death, respectively.
    PMID: 19956840 [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=3057612</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:52 +0100</pubDate>
            <guid isPermaLink="false">3057612</guid>        </item>
        <item>
            <title>Anti-tumor effect of apicidin on Ishikawa human endometrial cancer cells both in vitro and in vivo by blocking histone deacetylase 3 and 4.</title>
            <link>http://www.medworm.com/index.php?rid=3057611&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%3D19956841%26dopt%3DAbstract</link>
            <description>This study examined the anti-tumor effect of apicidin on human endometrial cancer Ishikawa cells in an animal model by inhibiting specific HDAC expression. Nude mice were injected subcutaneously (s.c.) with Ishikawa cells, and the levels of cell proliferation and apoptosis were measured in the tumor tissues after an apicidin treatment. The expression patterns of a specific HDAC class by apicidin were measured in Ishikawa endometrial cancer both in vitro and in vivo. The tumor volume and weight were measured after the apicidin treatment. Apicidin significantly increased the acetylated histone H3 levels in an Ishikawa cells in vitro culture but the levels of HDAC3 and HDAC4 expression were significantly decreased. Apicidin suppressed the tumor growth of transplanted Ishikawa cells, the expre...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057611</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:50 +0100</pubDate>
            <guid isPermaLink="false">3057611</guid>        </item>
        <item>
            <title>Exosomes derived from IL-12-anchored renal cancer cells increase induction of specific antitumor response in vitro: A novel vaccine for renal cell carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3057610&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%3D19956842%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Luo CL, He BC, Zhang JM, Cheng G, Wu XH
    Exosome-based immunotherapy for cancer holds promise, but needs improvements, especially for tumor-derived exosomes. We investigated, whether exosomes derived from IL-12-anchored human renal cancer cells could enhance their immunogenicity and increase induction of specific antitumor response. A mammalian co-expression plasmid of glycolipid-anchored-IL-12 (GPI-IL-12) was constructed by subcloning IL-12A chain gene (P35 subunit) and a fusion gene containing GPI-anchor signal sequence of human placental alkaline phosphatase-1 (hPLAP-1) and IL-12B chain gene (P40 subunit) in pBudCE4.1. Then exosomes were prepared from renal cancer cells modified to express GPI-IL-12. The results showed that exosomes derived from IL-12-anchored renal...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057610</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:47 +0100</pubDate>
            <guid isPermaLink="false">3057610</guid>        </item>
        <item>
            <title>Overexpression of HOXB7 homeobox gene in oral cancer induces cellular proliferation and is associated with poor prognosis.</title>
            <link>http://www.medworm.com/index.php?rid=3057609&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%3D19956843%26dopt%3DAbstract</link>
            <description>Authors: De Souza Setubal Destro MF, Bitu CC, Zecchin KG, Graner E, Lopes MA, Kowalski LP, Coletta RD
    A growing body of evidence has confirmed the involvement of dysregulated expression of HOX genes in cancer. HOX genes are a family of 39 transcription factors, divided in 4 clusters (HOXA to HOXD), that during normal development regulate cell proliferation and specific cell fate. In the present study it was investigated whether genes of the HOXB cluster play a role in oral cancer. We showed that most of the genes in the HOXB network are inactive in oral tissues, with exception of HOXB2, HOXB7 and HOXB13. Expression of HOXB7 was significantly higher in oral squamous cell carcinomas (OSCC) compared to normal oral mucosas. We further demonstrated that HOXB7 overexpression in HaCAT human e...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057609</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:43 +0100</pubDate>
            <guid isPermaLink="false">3057609</guid>        </item>
        <item>
            <title>Expression of Epstein-Barr nuclear antigen 1 in gastric carcinoma cells is associated with enhanced tumorigenicity and reduced cisplatin sensitivity.</title>
            <link>http://www.medworm.com/index.php?rid=3057608&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%3D19956844%26dopt%3DAbstract</link>
            <description>Authors: Cheng TC, Hsieh SS, Hsu WL, Chen YF, Ho HH, Sheu LF
    Epstein-Barr nuclear antigen 1 (EBNA-1) is consistently expressed in all EBV-associated gastric carcinomas. We explored its biological effects in gastric carcinoma cells by expressing the protein in two Epstein-Barr virus (EBV)-negative gastric carcinoma cell lines (SCM1 and TMC1). EBNA1-expressing SCM1 and TMC1 cells displayed no significant differences in growth rates, respectively, compared to those of vector-transfected SCM1 and TMC1 cells in vitro. However, EBNA1 was able to enhance tumorigenicity, the growth rate and the malignant histopathological grade in a xenograft nude mice test. We also evaluated whether EBNA1 caused EBNA1-expressing cells to have enhanced tumorigenicity in an immunocompetent host. We showed that ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057608</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:40 +0100</pubDate>
            <guid isPermaLink="false">3057608</guid>        </item>
        <item>
            <title>Hypoxia-induced des-gamma-carboxy prothrombin production in hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3057607&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%3D19956845%26dopt%3DAbstract</link>
            <description>Authors: Murata K, Suzuki H, Okano H, Oyamada T, Yasuda Y, Sakamoto A
    Des-gamma-carboxy prothrombin (DCP) is an established HCC tumor marker, but the precise mechanism of its production is still unclear. Recently, we demonstrated that cytoskeletal changes during epithelial-to-fibroblastoid conversion (EFC) or epithelial mesenchymal transition (EMT) induced by chemicals plays a critical mechanistic role in DCP production via impairment in vitamin K uptake. Our proposed mechanism of DCP production is consistent with substantial clinical evidence. Supplementary vitamin K2 analogues reduced serum DCP levels in hepatocellular carcinoma (HCC) patients. HCC patients with high serum DCP are associated with vascular invasion, metastasis and tumor recurrence. On the other hand, hypoxia has been ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057607</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:37 +0100</pubDate>
            <guid isPermaLink="false">3057607</guid>        </item>
        <item>
            <title>Frequent aberrant methylation of the imprinted IGF2/H19 locus and LINE1 hypomethylation in ovarian carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3057606&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%3D19956846%26dopt%3DAbstract</link>
            <description>Authors: Dammann RH, Kirsch S, Schagdarsurengin U, Dansranjavin T, Gradhand E, Schmitt WD, Hauptmann S
    Epigenetic alteration of tumor-related genes through changes of DNA methylation is a hallmark for carcinogenesis and aberrant DNA methylation modulates the activity of tumor suppressor genes, imprinted genes and repetitive elements. In ovarian carcinoma, frequent loss of imprinting or aberrant methylation of repetitive elements were reported, however, combined analysis were not performed. We analyzed the aberrant methylation of a differentially methylated region (DMR0) and a CTCF binding site of the IGF2-H19 locus and methylation of LINE1 and Satellite 2 in 22 primary ovarian carcinomas (OC) and controls by a quantitative bisulfite restriction analysis (QUBRA). In 91% of OC, a signifi...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057606</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:35 +0100</pubDate>
            <guid isPermaLink="false">3057606</guid>        </item>
        <item>
            <title>ICAM-3 enhances the migratory and invasive potential of human non-small cell lung cancer cells by inducing MMP-2 and MMP-9 via Akt and CREB.</title>
            <link>http://www.medworm.com/index.php?rid=3057605&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%3D19956847%26dopt%3DAbstract</link>
            <description>In this study, we hypothesized that ICAM-3 has an additional effect on cancer cell migration and invasion because molecules induced by ICAM-3 are known as regulators of cell migration and invasion. To examine this hypothesis, we used NCI-H1299 non-small cell lung cancer (NSCLC) cell line (p53 and PTEN null cell) and constructed an ICAM-3-over-expressing stable transfectant, which exhibited increased cell migration and invasion. The increased migration and invasion resulted from up-regulation of expression and activities of MMP-2 and MMP-9. ICAM-3 also increased Akt phosphorylation, which caused an increase in cellular migration/invasion and MMP activities. Activity of several transcriptional factors located downstream in the Akt pathway was also tested, and constitutive activation of adeno...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057605</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:32 +0100</pubDate>
            <guid isPermaLink="false">3057605</guid>        </item>
        <item>
            <title>N-glycosylation status of beta-haptoglobin in sera of patients with prostate cancer vs. benign prostate diseases.</title>
            <link>http://www.medworm.com/index.php?rid=3057604&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%3D19956848%26dopt%3DAbstract</link>
            <description>Authors: Yoon SJ, Park SY, Pang PC, Gallagher J, Gottesman JE, Dell A, Kim JH, Hakomori SI
    N-glycosylation status of purified beta-haptoglobin separated from sera of patients with prostate cancer was studied in comparison to that of sera from patients with benign prostate diseases, or normal subjects. Two different approaches, as summarized below, one based on binding of lectins and antibodies to beta-haptoglobin, the other on mass spectrometry of released N-linked glycans from beta-haptoglobin, were performed. Some of the results were useful for distinction of prostate cancer vs. benign prostate diseases. i) Binding of Phaseolus vulgaris-L lectin (PHA-L), defining the GlcNAcbeta6Manalpha6Man side chain present in tri- or tetra-antennary N-linked glycans, to beta-haptoglobin was higher...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057604</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:30 +0100</pubDate>
            <guid isPermaLink="false">3057604</guid>        </item>
        <item>
            <title>The assessment of methylated BASP1 and SRD5A2 levels in the detection of early hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=3057603&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%3D19956849%26dopt%3DAbstract</link>
            <description>Authors: Tsunedomi R, Ogawa Y, Iizuka N, Sakamoto K, Tamesa T, Moribe T, Oka M
    We previously identified BASP1 and SRD5A2 as novel hepatocellular carcinoma (HCC) methylation markers from among more than 10,000 screened genes. The present study aimed to improve the diagnostic potential of these genes. We compared the methylation status at distinct regions of the BASP1 and SRD5A2 genes using quantitative methylation-specific PCR, in 46 sets of HCC and corresponding non-tumor liver tissues. We also examined how their epigenetic status affected transcript levels in tissues and several hepatoma cell lines. We found that BASP1 and SRD5A2 loci were methylated in greater than 50% of the HCC tissues. Inverse correlations were identified between the methylation status and transcript levels in the...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057603</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:27 +0100</pubDate>
            <guid isPermaLink="false">3057603</guid>        </item>
        <item>
            <title>Pharmacokinetics, biodistribution and metabolism of a novel selective androgen receptor modulator designed for prostate cancer imaging.</title>
            <link>http://www.medworm.com/index.php?rid=3057602&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%3D19956850%26dopt%3DAbstract</link>
            <description>In conclusion, the extensive plasma clearance and de-iodination of S-26 likely contribute to its lack of AR tissue selectivity in vivo. Future studies using metabolically stable ligands with less lipophilicity and higher AR binding affinity may represent a promising and rational approach for AR-mediated imaging.
    PMID: 19956850 [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=3057602</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:24 +0100</pubDate>
            <guid isPermaLink="false">3057602</guid>        </item>
        <item>
            <title>The peroxisome proliferator-activated receptor gamma ligands, pioglitazone and 15-deoxy-Delta12,14-prostaglandin J2, have antineoplastic effects against hepatitis B virus-associated hepatocellular carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=3057601&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%3D19956851%26dopt%3DAbstract</link>
            <description>This study investigated the antineoplastic effects of intrinsic and extrinsic peroxisome proliferator-activated receptor gamma (PPARgamma) ligands against HBV-associated HCC cells in vitro. Four cell lines that were established from patients with HBV-associated HCC were used. The cells were cultured in various concentrations of the following PPARgamma ligands: troglitazone, pioglitazone, rosiglitazone and 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2). Cell proliferation, cell cycle and apoptosis were analyzed. PPARgamma was expressed in all the cell lines studied. Among the PPARgamma ligands, pioglitazone and 15d-PGJ2 clearly inhibited the HBV-associated HCC cell growth and increased the proportion of cells in the sub-G1 phase in the cell-cycle analysis. In apoptosis assays, DNA fragment...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057601</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:22 +0100</pubDate>
            <guid isPermaLink="false">3057601</guid>        </item>
        <item>
            <title>A fiber modified adenovirus vector that targets to the EphrinA2 receptor reveals enhanced gene transfer to ex vivo pancreatic cancer.</title>
            <link>http://www.medworm.com/index.php?rid=3057600&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%3D19956852%26dopt%3DAbstract</link>
            <description>We report the successful incorporation into the HI loop of peptide Tyr-Ser-Ala (YSA), a peptide ligand targeting the EphrinA2 (EphA2) receptor, and K237, a peptide targeting to the vascular endothelial growth factor receptor-II (VEGFRII). Subsequently, we showed that both peptides enhanced the transduction of a number of human PC lines that abundantly express the targeted receptor. Additional competition studies confirmed that the YSA peptide redirects Ad-YSA from CAR and specifically targets the EphA2 receptor. Due to this transduction efficiency of Ad-YSA is increased not only in human pancreatic cancer cell lines but more importantly also in pancreatic cancer resection specimens. Since the YSA peptide has been shown to specifically target pancreatic cancer in patients, it may be expecte...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057600</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:19 +0100</pubDate>
            <guid isPermaLink="false">3057600</guid>        </item>
        <item>
            <title>Loss of liver-intestine cadherin in human intrahepatic cholangiocarcinoma promotes angiogenesis by up-regulating metal-responsive transcription factor-1 and placental growth factor.</title>
            <link>http://www.medworm.com/index.php?rid=3057599&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%3D19956853%26dopt%3DAbstract</link>
            <description>In this study, we first examined LI-cadherin expression immunohistochemically in 34 specimens of human intrahepatic cholangiocarcinoma (ICC). LI-cadherin expression was positive (defined as positivity in &amp;gt;/=10% of cells) in 18 of the ICCs (52.9%). LI-cadherin negativity was significantly correlated with tumor dedifferentiation (P=0.026) and vascular invasion (P=0.015). The cumulative survival rate of patients with LI-cadherin-negative ICC was significantly shorter than that of patients with LI-cadherin-positive ICC (P=0.021). Multivariate analysis identified the extent of LI-cadherin staining as an independent prognostic factor for ICC survival (P=0.027). Next, to elucidate the mechanism of loss of LI-cadherin-mediated aggressiveness in ICC, we knocked down LI-cadherin expression in an ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057599</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:16 +0100</pubDate>
            <guid isPermaLink="false">3057599</guid>        </item>
        <item>
            <title>Alterations in a defined extracellular region of the RON receptor tyrosine kinase promote RON-mediated motile and invasive phenotypes in epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3057598&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%3D19956854%26dopt%3DAbstract</link>
            <description>This study determined the RON receptor in regulation of motile-invasive phenotypes of epithelial cells. Two RON variants, RON165.e11p and RON165, with alterations in a defined extracellular domain were used as the model. RON165 is a splicing variant generated by an mRNA transcript with an in-frame deletion of 49 amino acids encoded by exon 11. In contrast, RON165.e11p was produced by a partial deletion of exon 11 with the elimination of the first 40 amino acids. Thus, RON165.e11p differs from RON165 with nine amino acids retained in the fourth immunoglobulin-plexin-transcription (IPT) domain. Biochemically, both RON165 and RON165.e11p exist as a single-chain protein, residing in the cytoplasm, and failed to mature into the two-chain receptor. Both RON165 and RON165.e11p spontaneously forme...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057598</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:13 +0100</pubDate>
            <guid isPermaLink="false">3057598</guid>        </item>
        <item>
            <title>Comparative proteomic analysis of the esophageal squamous carcinoma cell line EC109 and its multi-drug resistant subline EC109/CDDP.</title>
            <link>http://www.medworm.com/index.php?rid=3057597&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%3D19956855%26dopt%3DAbstract</link>
            <description>Authors: Wen J, Zheng B, Hu Y, Zhang X, Yang H, Li Y, Zhang CY, Luo KJ, Zang X, Li YF, Guan XY, Fu JH
    To gain insights into the mechanisms of drug resistance in esophageal squamous cell carcinoma (ESCC), we employed proteomic techniques to study the global protein change of the multi-drug resistant ESCC cell line EC109/CDDP, which was established in our previous work, in comparison with its parental drug sensitive cell line EC109. By two-dimensional electrophoresis and mass spectrometry, we successfully identified 44 proteins with altered expression levels. These proteins are involved in endoplasmic reticulum stress response, metabolic process, DNA replication and repair, nucleotide binding, calcium binding, and cytoskeletal proteins. Among them, the differential expression levels of t...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057597</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:11 +0100</pubDate>
            <guid isPermaLink="false">3057597</guid>        </item>
        <item>
            <title>Expression of proteinase inhibitor-9/serpinB9 in non-small cell lung carcinoma cells and tissues.</title>
            <link>http://www.medworm.com/index.php?rid=3057596&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%3D19956856%26dopt%3DAbstract</link>
            <description>Authors: Rousalova I, Krepela E, Prochazka J, Cermak J, Benkova K
    Human proteinase inhibitor-9 (PI-9)/serpinB9 is an intracellular ovalbumin-family serpin with nucleocytoplasmic distribution which is expressed in certain normal cell types and cancer cells of different origin. Due to binding and inactivating of granzyme B (GrB), PI-9 can protect the cells from GrB-mediated apoptosis. High levels of PI-9 expression in certain cancer cells may contribute to their resistance against the immune mediated killing. So far, it is not known whether non-small cell lung cardinomas (NSCLCs) express PI-9 mRNA and a functional PI-9 protein. Herein we report for the first time that NSCLC cells express both PI-9 mRNA and protein and that there is a subset of NSCLC cells with upregulated PI-9 mRNA and p...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3057596</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:08 +0100</pubDate>
            <guid isPermaLink="false">3057596</guid>        </item>
        <item>
            <title>Cell cycle effects of fatty acid derivatives of cytarabine, CP-4055, and of gemcitabine, CP-4126, as basis for the interaction with oxaliplatin and docetaxel.</title>
            <link>http://www.medworm.com/index.php?rid=3057595&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%3D19956857%26dopt%3DAbstract</link>
            <description>In conclusion, the combinations with oxaliplatin showed a synergistic effect in the combination studies. Although the combinations with docetaxel did not show an enhanced effect in the in vitro studies, this combination revealed an increased effect in the xenograft model.
    PMID: 19956857 [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=3057595</comments>
            <pubDate>Sat, 05 Dec 2009 13:32:05 +0100</pubDate>
            <guid isPermaLink="false">3057595</guid>        </item>
        <item>
            <title>Activation of two distinct MAPK pathways governs constitutive expression of matrix metalloproteinase-1 in human pancreatic cancer cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=2963640&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%3D19885545%26dopt%3DAbstract</link>
            <description>This study contributes to provide new insights into strategies for inhibiting tumor cell invasion in pancreatic cancer.
    PMID: 19885545 [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=2963640</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:25 +0100</pubDate>
            <guid isPermaLink="false">2963640</guid>        </item>
        <item>
            <title>Bcr-Abl fusion sequences do not induce immune responses in mice when administered in mouse polyomavirus based virus-like particles.</title>
            <link>http://www.medworm.com/index.php?rid=2963639&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%3D19885546%26dopt%3DAbstract</link>
            <description>Authors: Hruskov&amp;#xE1; V, Mor&amp;#xE1;vkov&amp;#xE1; A, Babiarov&amp;#xE1; K, Ludv&amp;#xED;kov&amp;#xE1; V, Fric J, Vonka V, Forstov&amp;#xE1; J
    Mouse polyomavirus-like particles (MPyV-VLPs) carrying inside a fragment of the Bcr-Abl hybrid protein containing the epitope of chronic myeloid leukemia fusion region were prepared. A sequence encoding 171 amino acids covering Bcr-Abl breakpoint was fused to the C-terminal part of VP3 minor protein connecting it to the VP1 capsomeres. Chimeric particles, the Bcr-Abl VLPs, were tested for their ability to induce Bcr-Abl specific immune response in mice after their intranasal (i.n.) or intraperitoneal (i.p.) administration without any other adjuvants. Bcr-Abl VLPs induced strong anti-VP1 immune response in both i.n. and i.p. immunized mice. As expected, neither IgG ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963639</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:22 +0100</pubDate>
            <guid isPermaLink="false">2963639</guid>        </item>
        <item>
            <title>Targeted disruption of S100P suppresses tumor cell growth by down-regulation of cyclin D1 and CDK2 in human hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=2963638&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%3D19885547%26dopt%3DAbstract</link>
            <description>In conclusion, this study showed over-expression of S100P in HCC. The aberrant regulation of S100P in HCC might activate cyclin D1 and CDK expression and contribute to the mitogenic potential of tumor cells during HCC carcinogenesis. These findings provide information that suggests new therapeutic strategies for the treatment of liver cancer.
    PMID: 19885547 [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=2963638</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:20 +0100</pubDate>
            <guid isPermaLink="false">2963638</guid>        </item>
        <item>
            <title>Use of genetically engineered bone marrow-derived mesenchymal stem cells for glioma gene therapy.</title>
            <link>http://www.medworm.com/index.php?rid=2963637&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%3D19885548%26dopt%3DAbstract</link>
            <description>Authors: Amano S, Li S, Gu C, Gao Y, Koizumi S, Yamamoto S, Terakawa S, Namba H
    In our previous study, we successfully treated an established C6 brain tumor using neural stem cells transduced with the herpes simplex virus-thymidine kinase gene (HSVtk) and ganciclovir in the rat. In the present study, we investigated the use of mesenchymal stem cells (MSCs), obtained from adult rats and transduced with HSVtk (MSCtk cells), instead of neural stem cells because MSCs are much easier to obtain from the adult subjects. Those cells were used for in vitro co-culture study and in vivo co-implantation study with C6 rat glioma cells to examine bystander tumoricidal effect, which revealed a sufficient bystander effect and only 1/32 MSCtk cells were needed for complete tumor eradication. In vitro b...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963637</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:17 +0100</pubDate>
            <guid isPermaLink="false">2963637</guid>        </item>
        <item>
            <title>Localization of cortactin is associated with colorectal cancer development.</title>
            <link>http://www.medworm.com/index.php?rid=2963636&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%3D19885549%26dopt%3DAbstract</link>
            <description>Authors: Hirakawa H, Shibata K, Nakayama T
    Cortactin is a ubiquitously expressed actin filament (F-actin)-binding protein that stabilizes F-actin networks and promotes actin polymerization by activating the actin-related protein 2/3 (Arp2/3) complex. Overexpression of cortactin in cancer cells stimulate cell migration, invasion, and experimental metastasis; however, the underlying mechanism in cortactin involvement in tumor progression is not fully understood. Recently, a direct interaction between zonula occludens-1 (ZO-1) and cortactin in epithelial cells was reported. The present study aimed to further clarify the significance of the interaction between cortactin and ZO-1 in cancer progression. Cortactin expression and localization in colorectal human cancer tissues were evaluated b...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963636</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:15 +0100</pubDate>
            <guid isPermaLink="false">2963636</guid>        </item>
        <item>
            <title>alpha-tocopheryl phosphate suppresses tumor invasion concurrently with dynamic morphological changes and delocalization of cortactin from invadopodia.</title>
            <link>http://www.medworm.com/index.php?rid=2963635&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%3D19885550%26dopt%3DAbstract</link>
            <description>Authors: Saitoh Y, Yumoto A, Miwa N
    alpha-tocopheryl phosphate (TocP) has been elucidated for diverse effectiveness through unequivocal mechanisms independent of its conversion to alpha-tocopherol (Toc). The present study showed that TocP, in a dose-dependent manner, repressed invasion of human fibrosarcoma HT-1080 cells through the basement membrane, more markedly than Toc and several other Toc derivatives, although no cytotoxic effect was shown in either HT-1080 cells or human skin dermal fibroblastic cells DUMS-16. TocP diminished intracellular reactive oxygen species such as peroxides, lipid hydroperoxides and superoxide anion radicals in HT-1080 cells, but the effects were nearly equal or less than those of Toc. TocP suppressed either the cell motility or adhesion to extracellular...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963635</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:12 +0100</pubDate>
            <guid isPermaLink="false">2963635</guid>        </item>
        <item>
            <title>Dysregulation of the cell survival/anti-apoptotic NF-kappaB pathway by the novel humanized BM-ca anti-CD20 mAb: implication in chemosensitization.</title>
            <link>http://www.medworm.com/index.php?rid=2963634&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%3D19885551%26dopt%3DAbstract</link>
            <description>The objective of this study was to develop novel and fully humanized anti-CD20 monoclonal antibodies with enhanced effector functions and molecular signaling that may potentiate their therapeutic efficacy. Novel humanized anti-CD20 monoclonal antibodies were derived from a chimerized form of murine anti-CD20 1K11791, shown to exert a more potent ADCC, CDC and apoptotic activities compared to rituximab. A representative humanized monoclonal antibody, BM-ca was used to examine its biological effect and molecular signaling using Ramos B-NHL cell line as a model. The studies were also performed in parallel with rituximab treatment for comparison. Ramos cells were treated with various concentrations of BM-ca monoclonal antibody. Inhibition of cell proliferation was observed in a concentration-d...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963634</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:09 +0100</pubDate>
            <guid isPermaLink="false">2963634</guid>        </item>
        <item>
            <title>Cigarette smoke-induced DNA damage and repair detected by the comet assay in HPV-transformed cervical cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963633&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%3D19885552%26dopt%3DAbstract</link>
            <description>Authors: Moktar A, Ravoori S, Vadhanam MV, Gairola CG, Gupta RC
    Human papillomavirus (HPV) is the causative factor in the development and progression of cervical cancers in &amp;gt;97% of the cases, although insufficient. Epidemiological studies suggest an elevated risk of cervical cancer for cigarette smokers; therefore, we examined cigarette smoke-induced DNA damage and repair in HPV16-transformed human ectocervical cells (ECT1/E6 E7). Cells were treated with cigarette smoke condensate (CSC) for 72 h to assess the formation of single- and double-strand DNA breaks, measured by alkaline and neutral single cell gel electrophoresis assays, respectively. The mean tail length of cells with single-strand breaks was increased by 1.8-, 2.7- and 3.7-fold (p&amp;lt;0.001) after treatment with 4, 8 and ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963633</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:06 +0100</pubDate>
            <guid isPermaLink="false">2963633</guid>        </item>
        <item>
            <title>Inhibition of endothelial cell chemotaxis toward FGF-2 by gefitinib associates with downregulation of Fes activity.</title>
            <link>http://www.medworm.com/index.php?rid=2963632&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%3D19885553%26dopt%3DAbstract</link>
            <description>Authors: Kanda S, Naba A, Miyata Y
    Gefitinib inhibits epidermal growth factor-independent angiogenesis, but the molecular mechanism underlying this inhibition has yet to be defined. Here we show that gefitinib dose-dependently inhibited chemotaxis of endothelial cells toward fibroblast growth factor-2 (FGF-2), but not toward vascular endothelial growth factor-A (VEGF-A). Gefitinib inhibited lamellipodium formation by endothelial cells induced by FGF-2, but not by VEGF-A. Gefitinib at 10 microM did not inhibit autophosphorylation of FGF receptor 1 or VEGF receptor 2. A non-receptor protein tyrosine kinase, Fes, has two coiled-coil domains (CCDs) in its N-terminal region. Fes is activated by trans-autophosphorylation through CCD functions. An inactivating mutation in the second CCD aboli...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963632</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:04 +0100</pubDate>
            <guid isPermaLink="false">2963632</guid>        </item>
        <item>
            <title>Risk of gastric cancer is associated with the MUC1 568 A/G polymorphism.</title>
            <link>http://www.medworm.com/index.php?rid=2963631&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%3D19885554%26dopt%3DAbstract</link>
            <description>Authors: Xu Q, Yuan Y, Sun LP, Gong YH, Xu Y, Yu XW, Dong NN, Lin GD, Smith PN, Li RW
    Identifying the genetic variants that alter MUC1 protein expression may further our understanding of the risk for development of gastric cancer (GC). We used PCR-SSPs to identify the genotype of MUC1 A/G polymorphism at its 568 site of exon 2 and immunohistochemistry to detect MUC1 protein expression in GC patients and non-cancer subjects and analyzed the association between this polymorphism and MUC1 protein expression. We found that the frequency of AA genotype was significantly high in the GC patients and the risk for GC in AA genotype carriers increased 1.81-fold. Moreover, we found a significant underexpression of MUC1 protein in GC as compared to non-cancer subjects, which was negatively correla...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963631</comments>
            <pubDate>Thu, 05 Nov 2009 22:17:01 +0100</pubDate>
            <guid isPermaLink="false">2963631</guid>        </item>
        <item>
            <title>Gene expression profiling of archival tongue squamous cell carcinomas provides sub-classification based on DNA repair genes.</title>
            <link>http://www.medworm.com/index.php?rid=2963630&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%3D19885555%26dopt%3DAbstract</link>
            <description>Authors: Rentoft M, Laurell G, Coates PJ, Sj&amp;#xF6;str&amp;#xF6;m B, Nylander K
    A subgroup of patients with squamous cell carcinoma of the head and neck (SCCHN) comprise young persons under the age of 40, who have not been heavily exposed to the classical risk factors, smoking and alcohol. The number of SCCHN in young adults, particularly tongue tumours, is increasing in several parts of the world. Here we employed a novel gene expression array methodology specifically developed for analysis of degraded RNA and investigated the expression of 502 cancer-related genes in archival paraffin-embedded SCCHN of the tongue from young (&amp;lt; or =40) and elderly patients (&amp;gt; or =50). Genes detected as de-regulated in tumours compared to non-malignant controls were in concordance with results from ea...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963630</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:56 +0100</pubDate>
            <guid isPermaLink="false">2963630</guid>        </item>
        <item>
            <title>Oxidation of DJ-1-dependent cell transformation through direct binding of DJ-1 to PTEN.</title>
            <link>http://www.medworm.com/index.php?rid=2963629&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%3D19885556%26dopt%3DAbstract</link>
            <description>Authors: Kim YC, Kitaura H, Taira T, Iguchi-Ariga SM, Ariga H
    DJ-1 is an oncogene and also a causative gene for a familial form of Parkinson's disease. DJ-1 has multiple functions, including anti-oxidative stress reaction and cysteine 106 (C106) of DJ-1 is an essential amino acid for DJ-1 to exert its function. While increased expression and secretion of DJ-1 into serum in patients with various cancers and regulation of p53 and PTEN by DJ-1 have been reported, the molecular mechanism underlying oncogenicity of DJ-1 is poorly understood. Here, we analyzed the function of DJ-1 in the PI3'K signaling pathway under an oxidative stress condition, focusing on the interaction of DJ-1 with PTEN. We found that both wild-type (wt) and C106S-DJ-1, a substitution mutant of DJ-1, directly bound to ...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963629</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:53 +0100</pubDate>
            <guid isPermaLink="false">2963629</guid>        </item>
        <item>
            <title>MicroRNAs that respond to histone deacetylase inhibitor SAHA and p53 in HCT116 human colon carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963628&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%3D19885557%26dopt%3DAbstract</link>
            <description>In conclusion, we identified several miRNAs whose expression was affected by both SAHA and p53. Many of the miRNAs showed dramatic changes and were predicted to target many mRNAs. Further studies will be needed to verify these predictions.
    PMID: 19885557 [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=2963628</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:51 +0100</pubDate>
            <guid isPermaLink="false">2963628</guid>        </item>
        <item>
            <title>A novel resveratrol analogue HS-1793 treatment overcomes the resistance conferred by Bcl-2 and is associated with the formation of mature PML nuclear bodies in renal clear cell carcinoma Caki-1 cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963627&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%3D19885558%26dopt%3DAbstract</link>
            <description>Authors: Jeong SH, Lee JS, Jeong NY, Kim TH, Yoo KS, Song S, Suh H, Kwon TK, Park BS, Yoo YH
    Bcl-2 protects cancer cells from the apoptotic effects of various chemotherapeutic agents. Inhibition or downregulation of Bcl-2 represents a new therapeutic approach to bypass chemoresistance in cancer cells. Previously we designed and synthesized the resveratrol analogue HS-1793 displaying stronger antitumor efficacy than resveratrol and further demonstrated the HS-1793 resistance conferred by Bcl-2 in human leukemic U937 cells. We undertook this study to determine if HS-1793 treatment can bypass the anti-apoptotic effects of Bcl-2 in human renal cancer cells, with a specific focus on the involvement of promyelocytic leukemia nuclear bodies (PML-NBs). Experiments were conducted with Bcl-2-ove...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963627</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:48 +0100</pubDate>
            <guid isPermaLink="false">2963627</guid>        </item>
        <item>
            <title>AAV2-mediated interleukin-12 in the treatment of malignant brain tumors through activation of NK cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963626&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%3D19885559%26dopt%3DAbstract</link>
            <description>This study demonstrated an encouraging result of immunomodulative therapy in malignant brain tumors by rAAV2 carrying IL-12 through activating NK cells.
    PMID: 19885559 [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=2963626</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:46 +0100</pubDate>
            <guid isPermaLink="false">2963626</guid>        </item>
        <item>
            <title>Fatty acid synthase activity regulates HER2 extracellular domain shedding into the circulation of HER2-positive metastatic breast cancer patients.</title>
            <link>http://www.medworm.com/index.php?rid=2963625&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%3D19885560%26dopt%3DAbstract</link>
            <description>Authors: Vazquez-Martin A, Fernandez-Real JM, Oliveras-Ferraros C, Navarrete JM, Martin-Castillo B, Del Barco S, Brunet J, Menendez JA
    Clinicopathological assessment of the functional relationship between the HER2 oncogene and tumor-associated fatty acid synthase (FASN) is largely precluded because immunohistochemical and/or mRNA studies should be performed in biopsies from breast cancer patients. We here sought to determine whether serum FASN (sFASN) could associate with circulating HER2 extracellular domain (HER2 ECD) in the blood of metastatic breast cancer (MBC) patients. Concentrations of serum FASN and HER2 ECD were measured with ELISA in sera retrospectively obtained from 201 patients with metastatic breast cancer (MBC) and 31 healthy subjects. Mechanistical in vitro studies wer...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963625</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:43 +0100</pubDate>
            <guid isPermaLink="false">2963625</guid>        </item>
        <item>
            <title>Localization of telomerase hTERT protein in frozen sections of basal cell carcinomas (BCC) and tumor margin tissues.</title>
            <link>http://www.medworm.com/index.php?rid=2963624&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%3D19885561%26dopt%3DAbstract</link>
            <description>This study was supplemented with antibodies against Ki-67, nucleolin, common leucocyte antigen CD45 and mutated p53. The immunoreactive scores were determined and included the comparison with telomerase activity. The investigation of hTERT expression was performed in the tissues of 41 patients with BCC and control tissues of 14 patients without tumor. Eleven commercial antibodies were used for a nuclear staining of hTERT expression. With the anti-hTERT antibodies we looked for both satisfactory distribution and intensity of immunohistochemical labeling in the carcinomas and in the squamous epithelia of the tumor centers, of the tumor-free margins and of the control tissues. The hTERT expression in the BCC was distributed heterogeneously. The score values established by the anti-hTERT antib...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963624</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:40 +0100</pubDate>
            <guid isPermaLink="false">2963624</guid>        </item>
        <item>
            <title>Microarray gene expression profiling in meningiomas: differential expression according to grade or histopathological subtype.</title>
            <link>http://www.medworm.com/index.php?rid=2963623&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%3D19885562%26dopt%3DAbstract</link>
            <description>Authors: F&amp;#xE8;vre-Montange M, Champier J, Durand A, Wierinckx A, Honnorat J, Guyotat J, Jouvet A
    Meningiomas, one of the largest subgroup of intracranial tumours are generally benign, but can progress to malignancy. They are classified into the three World Health Organization grades: benign, atypical and anaplastic meningiomas. Various histopathological features have been associated with aggressiveness or recurrence. Several genes have been suggested as prognostic factors, but molecular signatures have not permitted the classification of the tumours into the three grades. We have performed a microarray transcriptomic study on 17 meningiomas of different malignancy using CodeLink Uniset Human Whole Genome Bioarrays to try to distinguish the different grades and histopathological subty...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963623</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:37 +0100</pubDate>
            <guid isPermaLink="false">2963623</guid>        </item>
        <item>
            <title>Osteopontin splice variants differentially modulate the migratory activity of hepatocellular carcinoma cell lines.</title>
            <link>http://www.medworm.com/index.php?rid=2963622&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%3D19885563%26dopt%3DAbstract</link>
            <description>Authors: Chae S, Jun HO, Lee EG, Yang SJ, Lee DC, Jung JK, Park KC, Yeom YI, Kim KW
    Osteopontin (OPN, SPP1) is a secretory extracellular matrix protein that has been implicated in cancer-associated mechanisms such as metastasis, invasion and angiogenesis. Three OPN isoforms (OPN-a, -b and -c) derived from alternative splicing are known to exist, but their functional specificity remains unclear. Here, we found that the expression profile of OPN isoforms in hepatocellular carcinoma (HCC) cell lines and patient tissues were correlated with specific cellular phenotypes and tumorigenicity of HCC. Thus, SK-Hep1 cells with a robust migratory capacity dominantly expressed both OPN-a and -b, but non-migratory cell lines such as Hep3B and PLC/PRF/5 mainly expressed OPN-c. Moreover, tumor tissues...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963622</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:35 +0100</pubDate>
            <guid isPermaLink="false">2963622</guid>        </item>
        <item>
            <title>Deficient histone acetylation and excessive deacetylase activity as epigenomic marks of prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963621&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%3D19885564%26dopt%3DAbstract</link>
            <description>Authors: Cang S, Feng J, Konno S, Han L, Liu K, Sharma SC, Choudhury M, Chiao JW
    Aberrant epigenomic alterations include incorrect histone modifications involving altered expression of chromatin-modifying proteins. They contribute to gene silencing and carcinogenesis. The nature of the epigenomic alterations occurring with prostate cancer remains to be fully identified. The acetylation status of histone H3 in human prostate cancer cells was assessed with multiple acetylation sites at N-termini. In contrast to the non-malignant prostatic cell lines RC165N/h and RC170N/h which possess stem cell properties, cancer cell lines LNCaP, DU-145, and PC-3 were either not acetylated or reduced in density (50-70%), at N-termini lysines 9, 14, 18, and 23 of histone H3. Deficient acetylation of hist...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963621</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:32 +0100</pubDate>
            <guid isPermaLink="false">2963621</guid>        </item>
        <item>
            <title>Vasculogenic mimicry of human ovarian cancer cells: role of CD147.</title>
            <link>http://www.medworm.com/index.php?rid=2963620&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%3D19885565%26dopt%3DAbstract</link>
            <description>In this study, we found significant correlations between expression of CD147 in ovarian cancer cell lines and tumor invasiveness, the activity of the proteases and the ability to form vascular channels. The treatment of SKOV3 cells with small interfering RNA against CD147 suppressed the ability of these cells to generate non-endothelial cell-lined channels. In contrast, transfection of CD147 cDNA into the CABA I cell line resulted in an increased tumor invasiveness and enabled the formation of vascular channels. Altogether, our data suggest that CD147 may play a critical role in VM of CABA I and SKOV3, human ovarian cancer cell lines.
    PMID: 19885565 [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=2963620</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:30 +0100</pubDate>
            <guid isPermaLink="false">2963620</guid>        </item>
        <item>
            <title>Cell density-dependent regulation of p73 in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963619&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%3D19885566%26dopt%3DAbstract</link>
            <description>Authors: Tophkhane C, Yang S, Zhao ZJ, Yang X
    Molecular regulation of p73, a p53 family member, remains unclear. Here we report that p73 expression is significantly regulated by cell densities. In particular, we found that p73alpha and p73beta are differentially regulated. While p73beta protein levels were inversely correlated with cell densities, p73alpha protein levels behaved oppositely. We further showed that density-dependent changes of p73alpha follow the same patterns as E2F-1 and TAp73 mRNA levels, suggesting transcriptional regulation. Our data also suggest that high levels of p73beta at lower densities may be due to increased protein stability. However, AIP-4/Itch appeared not to be involved in downregulation of p73beta at high densities. Moreover, we also found that subcellu...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963619</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:27 +0100</pubDate>
            <guid isPermaLink="false">2963619</guid>        </item>
        <item>
            <title>Thioredoxin2 enhances the damaged DNA binding activity of mtTFA through direct interaction.</title>
            <link>http://www.medworm.com/index.php?rid=2963618&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%3D19885567%26dopt%3DAbstract</link>
            <description>In this study, we found that expression levels of both mtTFA and the mitochondrial antioxidant protein thioredoxin2 (TRX2) are upregulated in cisplatin-resistant cell lines. In addition, TRX2 directly interacts with mtTFA and enhances its damaged DNA binding activity. The interaction between mtTFA and TRX2 requires the HMG box 1 motif of mtTFA. Furthermore, when amino acid substitutions were introduced at either C49G or C246stop, TRX2 interacted with mtTFA. However, the interaction of TRX2 with mtTFA was enhanced when both mutations (C49G and C246stop) were introduced. Binding to cisplatin-damaged DNA was similar among mutant mtTFA proteins. By contrast, binding to oxidized DNA was significantly enhanced when double mutations were introduced. These results suggest that TRX2 not only functi...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963618</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:25 +0100</pubDate>
            <guid isPermaLink="false">2963618</guid>        </item>
        <item>
            <title>Modulation of the transforming growth factor-beta1-induced Smad phosphorylation by the extracellular matrix receptor beta1-integrin.</title>
            <link>http://www.medworm.com/index.php?rid=2963617&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%3D19885568%26dopt%3DAbstract</link>
            <description>This study focuses on the alterations of the regulatory Smads (R-Smads) by TGF-beta1 in beta1-integrin-transfected HepG2 cells. The phosphorylation at the C-terminal site of R-Smads by TGF-beta1 was impaired in the beta1-integrin-transfected cells. However, the R-Smads were constitutively phosphorylated at the linker region in a MAP kinase-dependent manner. Furthermore, the expression of a mutant Smad3, that lacks the phosphorylation sites in the linker region, restored the TGF-beta1-induced Smad transcriptional activity. These results suggest that beta1-integrin impairs the TGF-beta1-mediated signals through the altered phosphorylation of the R-Smads.
    PMID: 19885568 [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=2963617</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:21 +0100</pubDate>
            <guid isPermaLink="false">2963617</guid>        </item>
        <item>
            <title>Increased expression of inhibitor of apoptosis proteins, survivin and XIAP, in non-small cell lung carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=2963616&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%3D19885569%26dopt%3DAbstract</link>
            <description>In conclusion, the overexpression of survivin in the majority of NSCLCs together with the abundant or upregulated expression of HBXIP and XIAP suggest that tumours are endowed with resistance against a variety of apoptosis-inducing conditions.
    PMID: 19885569 [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=2963616</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:19 +0100</pubDate>
            <guid isPermaLink="false">2963616</guid>        </item>
        <item>
            <title>The role of protein kinase C in the synergistic interaction of safingol and irinotecan in colon cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963615&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%3D19885570%26dopt%3DAbstract</link>
            <description>In this study, we investigated the anti-cancer effect of safingol as a single agent or in combination with irinotecan using HT-29 and LS-174T colon cancer cells as our in vitro models. As a single agent, safingol was more potent than irinotecan and 5-FU, with IC50 values of 2.5+/-1.1 microM and 3.4+/-1.0 microM achieved in HT-29 and LS-174T cells, respectively. However, protein kinase C (PKC) was not inhibited with concentrations of safingol which could induce substantial cell kill. The combination of safingol/irinotecan at 1:1 molar ratio was found to be additive in HT-29 cells (CI=0.94) and synergistic in LS-174T cells (CI=0.68), and resulted in concentration- and time-dependent down-regulation of p-PKC and p-MARCKS. The drug effect of the safingol/irinotecan combination was further modu...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2963615</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:16 +0100</pubDate>
            <guid isPermaLink="false">2963615</guid>        </item>
        <item>
            <title>Vascular endothelial growth inhibitor, expression in human prostate cancer tissue and the impact on adhesion and migration of prostate cancer cells in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=2963614&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%3D19885571%26dopt%3DAbstract</link>
            <description>In conclusion, the expression of VEGI is decreased in prostate cancer and is almost absent in tumours with high Gleason scores. Together with its inhibitory effect on cellular motility and adhesion, this suggests that VEGI functions as a negative regulator for aggressiveness during the development and progression of prostate cancer.
    PMID: 19885571 [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=2963614</comments>
            <pubDate>Thu, 05 Nov 2009 22:16:13 +0100</pubDate>
            <guid isPermaLink="false">2963614</guid>        </item>
        <item>
            <title>Novel 8-hydroxylquinoline analogs induce copper-dependent proteasome inhibition and cell death in human breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=2963613&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%3D19885572%26dopt%3DAbstract</link>
            <description>We report that when substitutions are made on the hydroxyl group of 8-OHQ, their copper mixtures have profound effects on the proteasome-inhibitory and apoptosis-inducing abilities in breast cancer MDA-MB-231 cells. In addition, the proteasome-inhibitory and apoptosis-inducing activities of 8-OHQ analog-copper mixtures are determined by both the polarity and position of the substituents. Finally, a synthetic complex of 8-OHQ analog-copper was able to inhibit the proteasome activity, induce cell death and suppress the growth selectively in breast cancer MDA-MB-231 cells, but not in normal immortalized human breast MCF-10A cells. Our results support the concept that human cancer cells and tissues, which contain an elevated copper level and are highly dependent on proteasome activity for thei...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
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            <pubDate>Thu, 05 Nov 2009 22:16:11 +0100</pubDate>
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            <title>The adenoviral E1A oncoprotein activates the Smad7 promoter: requirement of a functional E-box.</title>
            <link>http://www.medworm.com/index.php?rid=2963612&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%3D19885573%26dopt%3DAbstract</link>
            <description>In conclusion, these results unravel a novel mechanism of how the AdV E1A oncoprotein induces a cellular inhibitor of TGF-beta signalling.
    PMID: 19885573 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
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            <pubDate>Thu, 05 Nov 2009 22:16:08 +0100</pubDate>
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            <title>Induction of apoptosis in human colon cancer HCT-116 cells by anthocyanins through suppression of Akt and activation of p38-MAPK.</title>
            <link>http://www.medworm.com/index.php?rid=2963611&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%3D19885574%26dopt%3DAbstract</link>
            <description>In conclusion, this study suggests that the anthocyanins isolated from Vitis coignetiae Pulliat induce apoptosis might at least in part through activating p38-MAPK and suppressing Akt in human colon cancer HCT-116 cells.
    PMID: 19885574 [PubMed - in process] (Source: International Journal of Oncology)</description>
            <author>International Journal of Oncology</author>
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            <pubDate>Thu, 05 Nov 2009 22:16:06 +0100</pubDate>
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            <title>Immunophenotyping of diffuse large B-cell lymphoma (DLBCL) defines multiple sub-groups of germinal centre-like tumours displaying different survival characteristics.</title>
            <link>http://www.medworm.com/index.php?rid=2847784&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%3D19787248%26dopt%3DAbstract</link>
            <description>Authors: Anderson JJ, Fordham S, Overman L, Dignum H, Wood K, Proctor SJ, Crosier S, Angus B, Culpin RE, Mainou-Fowler T
    Diffuse large B-cell lymphoma (DLBCL) forms a heterogeneous collection of aggressive non-Hodgkin's Lymphoma in which three principle classes of neoplasia have been defined according to gene expression and immunophenotyping studies. The present investigation sought to examine the immunophenotype of proposed subgroups and relate these to patient survival. A series of 155 DLBCL treated uniformly with anthracycline therapy in clinical trials, were stratified upon the basis of common biomarker expression with combination immunophenotype being related to patient overall survival. Stratification of tumours with respect to combined expression profiles of the three biological...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
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            <pubDate>Thu, 01 Oct 2009 15:53:23 +0100</pubDate>
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            <title>Screening for genetic abnormalities involved in ovarian carcinogenesis using retroviral expression libraries.</title>
            <link>http://www.medworm.com/index.php?rid=2847783&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%3D19787249%26dopt%3DAbstract</link>
            <description>Authors: Wada T, Yamashita Y, Saga Y, Takahashi K, Koinuma K, Choi YL, Kaneda R, Fujiwara S, Soda M, Watanabe H, Kurashina K, Hatanaka H, Enomoto M, Takada S, Mano H, Suzuki M
    The purpose of this study was to screen for genes involved in ovarian carcinogenesis in an attempt to develop an effective molecular-targeted therapy for ovarian cancer. We constructed retroviral expression libraries for the human ovarian cancer cell lines SHIN-3 and TYK-CPr, and performed a focus formation assay with 3T3 cells. As a result, proteasome subunit beta-type 2 (PSMB2), ubiquitin-specific protease 14 (USP14), and keratin 8 (KRT8) were identified from SHIN-3, and polymerase II RNA subunit (POLR2E), chaperonin containing T-complex polypeptide 1 subunit 4 (CCT4), glia maturation factor beta (GMFB), and ne...</description>
            <author>International Journal of Oncology</author>
            <type>journals</type>
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            <pubDate>Thu, 01 Oct 2009 15:53:20 +0100</pubDate>
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            <title>Analysis of candidate target genes for mononucleotide repeat mutation in microsatellite instability-high (MSI-H) endometrial cancer.</title>
            <link>http://www.medworm.com/index.php?rid=2847782&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%3D19787250%26dopt%3DAbstract</link>
            <description>In this study, we analyzed mutations in 11 cancer-related genes with mononucleotide repeats susceptible to MSI in a coding region [hMSH3 (A8), hMSH6 (C8), TGF-beta RII (A10), MBD4 (A10), BAX (G8), PTEN (A6 in exon 7), HDAC2 (A9), EPHB2 (A9), Caspase-5 (A10), TCF-4 (A9) and Axin2 (G7)] in 22 patients with MSI-H sporadic endometrial cancer. Mutations in hMSH6 (C8) and TGF-beta RII (A10) were found most frequently, at rates of 36.3% (8/22) each. Mutations of BAX (G8) and TCF-4 (A9), which are common in MSI-positive colorectal cancer, occurred at rates of 22.7 and 0%, respectively, which suggests that the MSI target gene may differ between endometrial and colorectal cancers. Mutations in hMSH6 (C8) were correlated with reduced protein expression (p=0.042) and patients with these mutations had ...</description>
            <author>International Journal of Oncology</author>
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            <pubDate>Thu, 01 Oct 2009 15:53:18 +0100</pubDate>
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            <title>Does the expression of HPV16/18 E6/E7 in head and neck squamous cell carcinomas relate to their clinicopathological characteristics?</title>
            <link>http://www.medworm.com/index.php?rid=2847781&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%3D19787251%26dopt%3DAbstract</link>
            <description>We examined the expression of HPV16/18 E6/E7 in 71 cases of HNSCCs and investigated abnormalities of the p53 gene in 62 of these 71 cases. Expression of HPV16 E6/E7 was observed in 11 of the 71 cases (15.5%), while expression of HPV18 E6/E7 was not observed in any of the cases. Most of the HPV16 E6/E7-positive cases were histopathologically characterized by their verrucous or papillary structure and koilocytosis of the adjacent mucosa. There was no clear relationship between expression of HPV16 E6/E7 and tumor stage, prognosis or the positive rate of p53 abnormality. These results suggest that approximately 15% of HNSCCs are caused by HPV16 infection and the subsequent constitutive expression of E6 and E7, and that some HPV-initiated tumors lose their original characteristics during tumor ...</description>
            <author>International Journal of Oncology</author>
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            <pubDate>Thu, 01 Oct 2009 15:53:16 +0100</pubDate>
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