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        <title>Cancer Biology and Therapy 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 'Cancer Biology and Therapy' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Cancer+Biology+and+Therapy&t=Cancer+Biology+and+Therapy&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 08:41:19 +0100</lastBuildDate>
        <item>
            <title>Spermine synthase overexpression in vivo does not increase susceptibility to DMBA/TPA skin carcinogenesis or Min-Apc intestinal tumorigenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5624698&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22258329%26dopt%3DAbstract</link>
            <description>Authors: Welsh P, Sass-Kuhn S, Prakashagowda C, McCloskey D, Feith D
    Abstract
    Numerous studies have demonstrated a link between elevated polyamine biosynthesis and neoplastic growth, but the specific contribution of spermine synthase to epithelial tumor development has never been explored in vivo. Mice with widespread overexpression of spermine synthase (CAG-SpmS) exhibit decreased spermidine levels, increased spermine and a significant rise in tissue spermine:spermidine ratio. We characterized the response of CAG-SpmS mice to two-stage skin chemical carcinogenesis as well as spontaneous intestinal carcinogenesis induced by loss of the Apc tumor suppressor in ApcMin/+ (Min) mice. CAG-SpmS mice maintained the canonical increases in ornithine decarboxylase (ODC) activity, polyamine c...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624698</comments>
            <pubDate>Tue, 24 Jan 2012 21:12:20 +0100</pubDate>
            <guid isPermaLink="false">5624698</guid>        </item>
        <item>
            <title>Inhibition of STAT1 sensitizes renal cell carcinoma cells to radiotherapy and chemotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=5624697&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22262126%26dopt%3DAbstract</link>
            <description>Authors: Zhu H, Wang Z, Xu Q, Zhang Y, Zhai Y, Bai J, Liu M, Hui Z, Xu N
    Abstract
    Renal cell carcinoma is resistant to chemotherapy and radiotherapy. STAT1 is overexpressed in human RCC tissue. Downregulation of STAT1 expression could significantly increase the radiosensitivity in RCC cell lines. To further investigate the function of STAT1 in RCC resistance to chemoradiotherapy, a stable STAT1 knockdown cell line was established. Knockdown of STAT1 led to significant growth suppression in vitro and in vivo. Inhibition of STAT1 sensitized 786-O cells to radiotherapy and Taxol treatment. Cells with low STAT1 expression accumulated more strongly in the G2/M phase after treatment with chemotherapy and radiotherapy. The Human Cell Cycle and DNA Damage Signaling Pathway Real-time PCR ar...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5624697</comments>
            <pubDate>Tue, 24 Jan 2012 21:12:11 +0100</pubDate>
            <guid isPermaLink="false">5624697</guid>        </item>
        <item>
            <title>Thymosin beta 4 in colorectal cancer is localized predominantly at the invasion front in tumor cells undergoing epithelial mesenchymal transition.</title>
            <link>http://www.medworm.com/index.php?rid=5604178&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22233609%26dopt%3DAbstract</link>
            <description>Conclusions: Our data show that Tβ4 is expressed in the majority of colon cancers, with preferential immunoreactivity in deep tumor regions. The preferential expression of the peptide and the increase in intensity of the immunostaining at the invasion front suggests a possible link between the peptide and the process of epithelial mesenchymal transition, suggesting a role for Tβ4 in colorectal cancer invasion and metastasis.
    PMID: 22233609 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604178</comments>
            <pubDate>Thu, 19 Jan 2012 00:12:48 +0100</pubDate>
            <guid isPermaLink="false">5604178</guid>        </item>
        <item>
            <title>Fibroblast activation protein: A potential therapeutic target in cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5604177&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22236832%26dopt%3DAbstract</link>
            <description>Authors: Liu R, Li H, Liu L, Yu J, Ren X
    Abstract
    The concept of targeting antigens selectively expressed on the surface of tumor capillary endothelial cells or in tumor stroma has emerged as a promising strategy for cancer therapeutics. Identification of stromal targets  for anticancer therapy and development of selective inhibitors of these targets are of great clinical interest. Fibroblast activation protein (FAP), a member of the serine protease family, selectively expressed in the stromal fibroblasts associated with epithelial cancers, whereas with low or undetectable expression in the resting fibroblasts of normal adult tissues. The proteolytic activity of FAP has been shown to support tumor growth and proliferation, making it a potential target for novel anticancer...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604177</comments>
            <pubDate>Thu, 19 Jan 2012 00:12:39 +0100</pubDate>
            <guid isPermaLink="false">5604177</guid>        </item>
        <item>
            <title>Elevated expression of eukaryotic translation initiation factor 4E is associated with proliferation, invasion and acquired resistance to erlotinib in lung cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5604176&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22236867%26dopt%3DAbstract</link>
            <description>In this study, we detected increased levels of eIF4E in 16 human NSCLC cell lines compared with their normal bronchial epithelial cells. Consistently, human tissue array analysis showed that eIF4E expression was significantly higher in human NSCLC tissues than normal tissues. Inhibition of eIF4E using eIF4E siRNA inhibited the growth and invasion of NSCLC cells. These data suggest that eIF4E overexpression plays a crucial role in positive regulation of the growth and invasion of NSCLC cells. By proteomics, we found that eIF4E levels were elevated in erlotinib-resistant cell lines compared with the sensitive parental cell line. In agreement, assembly of the eIF4F cap complex and several oncogenic proteins regulated by the cap-dependent translation mechanism, were also increased in erlotinib...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604176</comments>
            <pubDate>Thu, 19 Jan 2012 00:12:30 +0100</pubDate>
            <guid isPermaLink="false">5604176</guid>        </item>
        <item>
            <title>HIPK2 downregulates vimentin and inhibits breast cancer cell invasion.</title>
            <link>http://www.medworm.com/index.php?rid=5604175&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22236966%26dopt%3DAbstract</link>
            <description>This study, by starting with a microarray analysis, demonstrates that HIPK2 downregulates vimentin expression in invasive, vimentin-positive, MDA-MB-231 breast cancer cells and in the non invasive MCF7 breast cancer cells subjected to chemical hypoxia, a drive for mesenchymal shift and tumor invasion. At functional level, vimentin downregulation by HIPK2 correlates with inhibition of breast tumor cell invasion. Together, these data show that vimentin is a novel target for HIPK2 repressor function and that HIPK2-mediated vimentin downregulation can contribute to inhibition of breast cancer cells invasion that might be applied in clinical therapy.
    PMID: 22236966 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604175</comments>
            <pubDate>Thu, 19 Jan 2012 00:12:21 +0100</pubDate>
            <guid isPermaLink="false">5604175</guid>        </item>
        <item>
            <title>MiRNA-21: A biomarker predictive for platinum-based adjuvant chemotherapy response in patients with non-small cell lung cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5604174&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22237007%26dopt%3DAbstract</link>
            <description>Conclusion: Our data suggests that the expression level of miR-21 in tumor tissue and plasma might be used as a biomarker to predict adjuvant platinum based chemotherapy response and disease free survival in patients with NSCLC. Thus, it may serve as a novel therapeutic target to modulate platinum-based chemotherapy.
    PMID: 22237007 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5604174</comments>
            <pubDate>Thu, 19 Jan 2012 00:12:12 +0100</pubDate>
            <guid isPermaLink="false">5604174</guid>        </item>
        <item>
            <title>Identification of mammary epithelial cells subject to chronic oxidative stress in mammary epithelium of young women and teenagers living in USA: Implication for breast carcinogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5578890&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231390%26dopt%3DAbstract</link>
            <description>Authors: Weisz J, Shearer DA, Murata E, Patrick SD, Han B, Berg A, Clawson GA
    Abstract
    Current knowledge of changes in the mammary epithelium relevant to breast carcinogenesis is limited to when histological changes are already present because of a lack of biomarkers needed to identify where such molecular changes might be ongoing at earlier during the of decades-long latent stages of breast carcinogenesis. Breast reduction tissues from young women and teenagers, representative of USA's high breast cancer incidence population, were studies using immunocytochemistry and targeted PCR arrays in order to learn whether a marker of chronic oxidative-stress [protein adducts of 4-hydroxy-2-nonenal (4HNE)] can identify where molecular changes relevant to carcinogenesis might be taking place...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578890</comments>
            <pubDate>Thu, 12 Jan 2012 04:00:43 +0100</pubDate>
            <guid isPermaLink="false">5578890</guid>        </item>
        <item>
            <title>Radiosensitization induced by the anti-epidermal growth factor receptor monoclonal antibodies cetuximab and nimotuzumab in A431 cells.</title>
            <link>http://www.medworm.com/index.php?rid=5578889&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231391%26dopt%3DAbstract</link>
            <description>Authors: González JE, Barquinero JF, Lee M, García O, Casacó A
    Abstract
    Epidermal growth factor receptors (EGFR) are over-expressed in a wide range of malignancies including head and neck, colon and breast cancers. It has been identified that carcinomas with high expression levels of EGFR are more resistant to radiotherapy. Therefore, inhibiting nuclear translocation of EGFR to increase the radiosensitivity of malignant cells expressing EGFR offers the potential for increasing the therapeutic index of radiotherapy. The purpose of the present study was to quantify and to compare the radiosensitizing properties of the well known anti-EGFR antibodies, cetuximab and nimotuzumab in human epidermoid A431 overexpressing EGFR cells. Cells were treated with two concentrations of the anti...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578889</comments>
            <pubDate>Thu, 12 Jan 2012 04:00:33 +0100</pubDate>
            <guid isPermaLink="false">5578889</guid>        </item>
        <item>
            <title>Dioscin induces cancer cell apoptosis through elevated oxidative stress mediated by downregulation of peroxiredoxins.</title>
            <link>http://www.medworm.com/index.php?rid=5578888&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231406%26dopt%3DAbstract</link>
            <description>In conclusion, we suggest that PRDX1 and PRDX6 are key targets in the process of dioscin-induced apoptosis that involves intracellular elevated ROS.
    PMID: 22231406 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578888</comments>
            <pubDate>Thu, 12 Jan 2012 04:00:22 +0100</pubDate>
            <guid isPermaLink="false">5578888</guid>        </item>
        <item>
            <title>Dietary calcium supplementation enhances efficacy but also toxicity of EGFR inhibitor therapy for colon cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5578887&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22231407%26dopt%3DAbstract</link>
            <description>Authors: Rinella E, Bankaitis E, Threadgill D
    Abstract
    The inverse correlation between levels of dietary calcium and colorectal cancer (CRC) incidence has been extensively investigated. However, the impact of supplemental calcium on cancer therapy remains unknown. We used four models of CRC, Caco-2 and HCT116 human cancer cell lines and ApcMin/+ and azoxymethane carcinogen-induced mouse models, to investigate the impact of a western-style diet low in calcium (0.05%) versus a similar diet but supplemented with calcium (5%) on therapeutic targeting of the epidermal growth factor receptor (EGFR). We found that calcium supplementation combined with pharmacologic blockade of EGFR results in an additive effect on tumor growth inhibition in all models. Unexpectedly, the combined use of di...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5578887</comments>
            <pubDate>Thu, 12 Jan 2012 04:00:12 +0100</pubDate>
            <guid isPermaLink="false">5578887</guid>        </item>
        <item>
            <title>Personalized therapy in endometrial cancer: Challenges and opportunities.</title>
            <link>http://www.medworm.com/index.php?rid=5550955&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198566%26dopt%3DAbstract</link>
            <description>Authors: Westin SN, Broaddus RR
    Abstract
    Early stage endometrial cancer is generally curable. However, progress in the treatment of advanced and recurrent endometrial cancer has been limited. This has led to a shift from the use of traditional chemotherapeutic agents and radiotherapy regimens to the promising area of targeted therapy, given the large number of druggable molecular alterations found in endometrial cancer. To maximize the effects of directed targeted therapy, careful molecular characterization of the endometrial tumor is necessary. This represents an important difference in the use of targeted therapy versus traditional chemotherapy or radiation treatment. This review will discuss relevant pathways to target in endometrial cancer as well as the challenges which arise ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550955</comments>
            <pubDate>Fri, 30 Dec 2011 12:06:21 +0100</pubDate>
            <guid isPermaLink="false">5550955</guid>        </item>
        <item>
            <title>EMMPRIN silencing inhibits proliferation and perineural invasion of human salivary adenoid cystic carcinoma cells in vitro and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5550954&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198615%26dopt%3DAbstract</link>
            <description>Authors: Yang X, Zhang P, Ma Q, Kong L, Li Y, Liu B, Lei D
    Abstract
    Salivary adenoid cystic carcinoma (SACC) is a frequent subtype of salivary gland malignancy, and it has an important biological behavior for perineural invasion (PNI). Extracellular matrix metalloproteinase inducer (EMMPRIN) is a transmembrane glycoprotein that is involved in the invasive property of many malignancies by stimulating matrix metalloproteinase (MMP) expression. The present study was designed to investigate the role and possible mechanism of EMMPRIN in the PNI of SACC using RNA interference (RNAi) technology. We found that silencing of EMMPRIN expression in the human SACC cell line (SACC-83) suppressed the cell proliferation, adhesion, MMP-2 and MMP-9 secretion, and PNI activity in vitro. EMMPRIN silen...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5550954</comments>
            <pubDate>Fri, 30 Dec 2011 12:06:13 +0100</pubDate>
            <guid isPermaLink="false">5550954</guid>        </item>
        <item>
            <title>Human prostate cancer ZIP1/zinc/citrate genetic/metabolic relationship in the TRAMP prostate cancer animal model.</title>
            <link>http://www.medworm.com/index.php?rid=5514639&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22156800%26dopt%3DAbstract</link>
            <description>Authors: Costello LC, Franklin RB, Zou J, Feng P, Bok R, Mark G S, Kurhanewicz J
    Abstract
    Prostate cancer is the second leading cause of cancer deaths among men. The availability of animal models that represent the events and factors that exist in the natural history and biology of human prostate cancer is essential in dealing with prostate cancer. In recent decades and presently, emphasis has been directed at the development and employment of prostate cancer induced in transgenic mice. However, the important consistent hallmark characteristic and event of decrease in zinc and citrate and down regulation of ZIP1 zinc transporter in prostate malignancy has not been studied or identified in any animal model. We investigated the status of these parameters in TRAMP tumors as compared t...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514639</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514639</guid>        </item>
        <item>
            <title>The Akt signaling pathway: An emerging therapeutic target in malignant melanoma.</title>
            <link>http://www.medworm.com/index.php?rid=5514638&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22157148%26dopt%3DAbstract</link>
            <description>Authors: Madhunapantula SV, Mosca PJ, Robertson GP
    Abstract
    Studies using cultured melanoma cells and patient tumor biopsies have demonstrated deregulated PI3 kinase-Akt3 pathway activity in ~70% of melanomas. Furthermore, targeting Akt3 and downstream PRAS40 has been shown to inhibit melanoma tumor development in mice. Although these preclinical studies and several other reports using small interfering RNAs and pharmacological agents targeting key members of this pathway have been shown to retard melanoma development, analysis of early Phase I and Phase II clinical trials using pharmacological agents to target this pathway demonstrate the need for (a) selection of patients whose tumors have PI3 kinase-Akt pathway deregulation, (b) further optimization of therapeutic agents for inc...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514638</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514638</guid>        </item>
        <item>
            <title>Cardiac and gastrointestinal liabilities caused by deficiency in the immune modulatory enzyme indoleamine 2,3-dioxygenase.</title>
            <link>http://www.medworm.com/index.php?rid=5514637&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22157149%26dopt%3DAbstract</link>
            <description>Authors: Chang MY, Smith C, Duhadaway JB, Pyle JR, Boulden J, Peralta Soler A, Muller AJ, Laury-Kleintop LD, Prendergast GC
    Abstract
    Indoleamine 2,3-dioxygenase (IDO) modifies adaptive immunity, in part, by determining the character of inflammatory responses in the tissue microenvironment. Small molecule inhibitors of IDO are being developed to treat cancer, chronic infections and other diseases, so the systemic effects of IDO disruption on inflammatory phenomena may influence the design and conduct of early phase clinical investigations of this new class of therapeutic agents. Here, we report cardiac and gastrointestinal phenotypes observed in IDO deficient mice that warrant consideration in planned assessments of the safety risks involved in clinical development of IDO inhibitors...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514637</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514637</guid>        </item>
        <item>
            <title>Aurora A mediates cross-talk between N- and C-terminal post-translational modifications of p53.</title>
            <link>http://www.medworm.com/index.php?rid=5514636&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22157150%26dopt%3DAbstract</link>
            <description>Authors: Warnock LJ, Raines SA, Milner J
    Abstract
    The serine/threonine protein kinase Aurora A is known to interact with and phosphorylate tumour suppressor p53 at Serine 215 (S215), inhibiting the transcriptional activity of p53. We show that Aurora A positively regulates human p53 protein levels and, using isogenic p53 wild-type and p53-null colorectal carcinoma cells, further show that p53 regulates human Aurora A protein expression. S215 is located in the DNA-binding core of p53 and at the center of the cryptic epitope for PAb240 antibody, which is used to detect mutant and denatured p53. Following denaturing SDS PAGE, the PAb240 epitope was detectable by immunoblotting in only two out of eight cell lines. The efficacy of novel p53-targeted anticancer therapies may be influence...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5514636</comments>
            <pubDate>Thu, 15 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5514636</guid>        </item>
        <item>
            <title>Tumor cell metabolism: An integral view.</title>
            <link>http://www.medworm.com/index.php?rid=5423407&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22057267%26dopt%3DAbstract</link>
            <description>Authors: Romero-Garcia S, Lopez-Gonzalez JS, Báez-Viveros JL, Aguilar-Cazares D, Prado-Garcia H
    Abstract
    Cancer is a genetic disease that is caused by mutations in oncogenes, tumor suppressor genes and stability genes. The fact that the metabolism of tumor cells is altered has been known for many years. However, the mechanisms and consequences of metabolic reprogramming have just begun to be understood. In this review, an integral view of tumor cell metabolism is presented, showing how metabolic pathways are reprogrammed to satisfy tumor cell proliferation and survival requirements. In tumor cells, glycolysis is strongly enhanced to fulfill the high ATP demands of these cells; glucose carbons are the main building blocks in fatty acid and nucleotide biosynthesis. Glutaminolysis is...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5423407</comments>
            <pubDate>Sat, 19 Nov 2011 11:54:21 +0100</pubDate>
            <guid isPermaLink="false">5423407</guid>        </item>
        <item>
            <title>Sorafenib increases endoplasmic reticulum (ER) stress in concert with vorinostat.</title>
            <link>http://www.medworm.com/index.php?rid=5423406&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22095133%26dopt%3DAbstract</link>
            <description>In this study, they found expression of PDGFRbeta and FLT3 were essential for high dose single agent sorafenib to promote autophagy. We would like to extend the discussion begun by Park et al. by introducing a route through which sorafenib could trigger the onset of molecular events causing cellular stress.
    PMID: 22095133 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5423406</comments>
            <pubDate>Sat, 19 Nov 2011 11:54:11 +0100</pubDate>
            <guid isPermaLink="false">5423406</guid>        </item>
        <item>
            <title>How can grafted breast cancer models be optimized?</title>
            <link>http://www.medworm.com/index.php?rid=5423408&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22057217%26dopt%3DAbstract</link>
            <description>Authors: Mollard S, Mousseau Y, Baaj Y, Richard L, Cook-Moreau J, Monteil J, Funalot B, Sturtz FG
    Abstract
    Breast cancer is the most frequent spontaneous malignancy diagnosed in women and is characterized by a broad histological diversity. Progression of the disease has a metastasizing trend and can be resistant to hormonal and chemotherapy. Animal models have provided some understanding of these features and have allowed new treatments to be proposed. However, these models need to be revised because they have some limitations in predicting the clinical efficacy of new therapies. In this review, we discuss the biological criteria to be taken into account for a realistic animal model of breast-cancer graft (tumor implantation site, animal immune status, histological diversity, moder...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5423408</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5423408</guid>        </item>
        <item>
            <title>Efficacy of therapy for hepatocellular carcinoma with portal vein tumor thrombus: Chemoembolization and stent combined with iodine-125 seed.</title>
            <link>http://www.medworm.com/index.php?rid=5381923&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22037354%26dopt%3DAbstract</link>
            <description>Authors: Chuan-Xing L, Xu H, Bao-Shan H, Yong L, Pei-Jian S, Xian-Yi Y, Xiao-Ning L, Li-Gong L
    Abstract
    The purpose of this study is to analyze the safety and clinical efficacy of transcatheter arterial chemoembolization (TACE) combined with portal vein stent and 125I implantation for the treatment of portal vein tumor thrombus (PVTT) in hepatocellular carcinoma. Fifty-six patients from our department diagnosed with advanced hepatocellular carcinoma with PVTT between January 2008 and December 30, 2010 were divided into two groups. Patients in Group A were treated with TACE and portal vein stent; Patients in Group B were treated with TACE, portal vein stent, and 125I implantation. The success rate of TACE with portal vein stent and 125I implantation was 100%, with no severe surgery-...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5381923</comments>
            <pubDate>Mon, 07 Nov 2011 10:25:35 +0100</pubDate>
            <guid isPermaLink="false">5381923</guid>        </item>
        <item>
            <title>Anti-estrogen resistance in breast cancer is induced by the tumor microenvironment and can be overcome by inhibiting mitochondrial function in epithelial cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5381922&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22041887%26dopt%3DAbstract</link>
            <description>Authors: Martinez-Outschoorn UE, Goldberg A, Lin Z, Ko YH, Flomenberg N, Wang C, Pavlides S, Pestell RG, Howell A, Sotgia F, Lisanti MP
    Abstract
    Here, we show that tamoxifen resistance is induced by cancer-associated fibroblasts (CAFs). Coculture of estrogen receptor positive (ER+) MCF7 cells with fibroblasts induces tamoxifen and fulvestrant resistance with 4.4- and 2.5-fold reductions, respectively, in apoptosis compared to homotypic MCF7 cell cultures. Treatment of MCF7 cells cultured alone with high-energy mitochondrial &quot;fuels&quot; (L-lactate or ketone bodies) is sufficient to confer tamoxifen resistance, mimicking the effects of coculture with fibroblasts. To further demonstrate that epithelial cancer cell mitochondrial activity is the origin of tamoxifen resistance, we employed c...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5381922</comments>
            <pubDate>Mon, 07 Nov 2011 10:25:25 +0100</pubDate>
            <guid isPermaLink="false">5381922</guid>        </item>
        <item>
            <title>Depletion of tissue factor suppresses hepatic metastasis and tumor growth in colorectal cancer via the downregulation of MMPs and the induction of autophagy and apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5381921&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22052255%26dopt%3DAbstract</link>
            <description>In conclusion, our data provide new insight into hepatic metastasis of CRC. Agents targeting TF should be developed as adjuvant therapeutics for CRC metastasis.
    PMID: 22052255 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5381921</comments>
            <pubDate>Mon, 07 Nov 2011 10:25:15 +0100</pubDate>
            <guid isPermaLink="false">5381921</guid>        </item>
        <item>
            <title>Knockdown of VEGF receptor-1 (VEGFR-1) impairs macrophage infiltration, angiogenesis and growth of clear cell renal cell rarcinoma (CRCC).</title>
            <link>http://www.medworm.com/index.php?rid=5361920&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21989163%26dopt%3DAbstract</link>
            <description>Authors: Li C, Liu B, Dai Z, Tao Y
    Abstract
    Angiogenesis is essential for tumor growth and metastasis. VEGF has been shown to be a central player in this process. The biological activity of VEGF is mainly mediated by two tyrosine kinase receptors, VEGFR-1 and VEGFR-2. While increasing evidence suggests that VEGF/VEGFR-1 signaling is crucial for tumor angiogenesis, its molecular mechanism is not well understood. Here we show that VEGFR-1 knockdown dramatically inhibits tumor growth. This inhibition is associated with significant decrease of tumor VEGF levels and tumor angiogenesis as well as an increased tumor necrosis. Moreover, we demonstrate that VEGF in CRCC tumors is mainly produced by tumor stromal cells instead of the tumor cells themselves. It has been shown that macrophages...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5361920</comments>
            <pubDate>Tue, 01 Nov 2011 09:10:57 +0100</pubDate>
            <guid isPermaLink="false">5361920</guid>        </item>
        <item>
            <title>Enhancement of specific cellular immune response induced by glycosyl-phosphatidylinositol-anchored BCR/ABL and mIL-12.</title>
            <link>http://www.medworm.com/index.php?rid=5361919&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024730%26dopt%3DAbstract</link>
            <description>In this study, we sought to enhance cellular immunity by co-expression of BCR/ABL and murine IL-12 gene on the tumor cell surface as a glycosyl-phosphatidylinositol (GPI)-form. The successfully constructed plasmid pBudCE4.1-BCR/ABL-GPI-mIL12 resulted in high levels of splenocyte proliferative responses, significant levels of IL-2 and IFN-γ, and strong cytotoxic T lymphocyte (CTL) responses in vitro. In a murine transplant model, the vaccinated mice showed decreased infiltration of leukemia cells and reduced expression of BCR/ABL transcripts and protein in bone marrow cells. Results of the present study indicated that this novel immunization strategy is useful in enhancing immune protection in mice, which would provide new insights into the development of effective vaccines for treating CM...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5361919</comments>
            <pubDate>Tue, 01 Nov 2011 09:10:46 +0100</pubDate>
            <guid isPermaLink="false">5361919</guid>        </item>
        <item>
            <title>Interferon γ improves the vaccination potential of oncolytic parvovirus H-1PV for the treatment of peritoneal carcinomatosis in pancreatic cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5361918&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024742%26dopt%3DAbstract</link>
            <description>Authors: Grekova SP, Aprahamian M, Daeffler L, Leuchs B, Angelova A, Giese T, Galabov A, Heller A, Giese NA, Rommelaere J, Raykov Z
    Abstract
    Oncolytic viruses with their capacity to specifically replicate in and kill tumor cells emerged as a novel class of cancer therapeutics. Rat oncolytic parvovirus (H-1PV) was used to treat different types of cancer in preclinical settings and was lately successfully combined with standard gemcitabine chemotherapy in treating pancreatic ductal adenocarcinoma (PDAC) in rats. Our previous work showed that the immune system and particularly the release of interferon-gamma (IFNγ ) seem to mediate the anticancer effect of H-1PV in that model. Therefore, we reasoned that the therapeutic properties of H-1PV can be boosted with IFNγ for the treatment ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5361918</comments>
            <pubDate>Tue, 01 Nov 2011 09:10:35 +0100</pubDate>
            <guid isPermaLink="false">5361918</guid>        </item>
        <item>
            <title>The effects of resveratrol and selected metabolites on the radiation and antioxidant response.</title>
            <link>http://www.medworm.com/index.php?rid=5361917&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024758%26dopt%3DAbstract</link>
            <description>Authors: Fabre KM, Saito K, Degraff W, Sowers AL, Thetford A, Cook JA, Krishna MC, Mitchell JB
    Abstract
    Excess reactive oxygen species (ROS) generated from ionizing radiation (IR) or endogenous sources like cellular respiration and inflammation produce cytotoxic effects that can lead to carcinogenesis. Resveratrol (RSV), a polyphenol with antioxidant and anticarcinogenic capabilities, has shown promise as a potential radiation modifier. The present study focuses on examining the effects of RSV or RSV metabolites as a radiation modifier in normal tissue. RSV or a RSV metabolite, piceatannol (PIC) did not protect human lung fibroblasts (1522) from the radiation-induced cell killing. Likewise, neither RSV nor PIC afforded protection against lethal total body IR in C3H mice. Additional...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5361917</comments>
            <pubDate>Tue, 01 Nov 2011 09:10:24 +0100</pubDate>
            <guid isPermaLink="false">5361917</guid>        </item>
        <item>
            <title>Inhibition of hypoxia-induced miR-155 radiosensitizes hypoxic lung cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5361916&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22027557%26dopt%3DAbstract</link>
            <description>Authors: Babar IA, Czochor J, Steinmetz A, Weidhaas JB, Glazer PM, Slack FJ
    Abstract
    miR-155 is a prominent microRNA (miRNA) that regulates genes involved in immunity and cancer-related pathways. miR-155 is overexpressed in lung cancer, which correlates with poor patient prognosis. It is unclear how miR-155 becomes increased in lung cancers and how this increase contributes to reduced patient survival. Here, we show that hypoxic conditions induce miR-155 expression in lung cancer cells and trigger a corresponding decrease in a validated target, FOXO3A. Furthermore, we find that increased levels of miR-155 radioprotects lung cancer cells, while inhibition of miR-155 radiosensitizes these cells. Moreover, we reveal a therapeutically important link between miR-155 expression, hypoxia,...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5361916</comments>
            <pubDate>Tue, 01 Nov 2011 09:10:13 +0100</pubDate>
            <guid isPermaLink="false">5361916</guid>        </item>
        <item>
            <title>Sunitinib-induced asthenia: from molecular basis to clinical relief.</title>
            <link>http://www.medworm.com/index.php?rid=5298905&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21968390%26dopt%3DAbstract</link>
            <description>This study considered different clinical observations and current metabolic and pharmacological knowledge, leading to hypotheses regarding which molecular mechanisms may be involved in sunitinib-induced AFS in cancer patients. Deeper knowledge of the molecular mode of action of sunitinib may lead to improved optimization of its clinical use.
    PMID: 21968390 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5298905</comments>
            <pubDate>Sun, 09 Oct 2011 20:25:10 +0100</pubDate>
            <guid isPermaLink="false">5298905</guid>        </item>
        <item>
            <title>Single nucleotide polymorphisms of ABCC5 and ABCG1 transporter genes correlate to irinotecan-associated gastrointestinal toxicity in colorectal cancer patients: A DMET microarray profiling study.</title>
            <link>http://www.medworm.com/index.php?rid=5219664&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21892003%26dopt%3DAbstract</link>
            <description>Authors: Di Martino MT, Arbitrio M, Leone E, Guzzi PH, Saveria Rotundo M, Ciliberto D, Tomaino V, Fabiani F, Talarico D, Sperlongano P, Doldo P, Cannataro M, Caraglia M, Tassone P, Tagliaferri P
    Abstract
    Recent findings have disclosed the role of UDP-glucuronosyltransferase (UGT) 1A1*28 on the haematological toxicity induced by irinotecan (CPT-11), a drug commonly used in the treatment of metastatic colorectal cancer (mCRC). We investigated the pharmacogenomic profile of irinotecan-induced gastrointestinal (GI) toxicity by the novel drug-metabolizing enzyme and transporter (DMET) microarray genotyping platform. Twenty-six mCRC patients who had undergone to irinotecan-based chemotherapy were enrolled in a case (patients experiencing &amp;gt; grade 3 gastrointestinal, (GI) toxicity) - co...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219664</comments>
            <pubDate>Thu, 15 Sep 2011 09:16:29 +0100</pubDate>
            <guid isPermaLink="false">5219664</guid>        </item>
        <item>
            <title>Chk1 inhibition and Wee1 inhibition combine synergistically to impede cellular proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=5219663&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21892012%26dopt%3DAbstract</link>
            <description>In conclusion, the clinical combination of a Chk1 inhibitor and a Wee1 inhibitor holds promise as an effective treatment strategy for cancer.
    PMID: 21892012 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219663</comments>
            <pubDate>Thu, 15 Sep 2011 09:16:20 +0100</pubDate>
            <guid isPermaLink="false">5219663</guid>        </item>
        <item>
            <title>C086, a novel analogue of curcumin, induces growth inhibition and down-regulation of NFκB in colon cancer cells and xenograft tumors.</title>
            <link>http://www.medworm.com/index.php?rid=5219662&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21900746%26dopt%3DAbstract</link>
            <description>In this study, the effects of C086 on growth inhibition and NFκB pathway regulation were investigated in colon cancer cells and xenograft tumors. C086 exhibited potent antiproliferative activity in all 6 colon cancer cell lines. In a xenograft model of SW480 cells in nude mice, the oral administration of C086 showed significant growth suppression of SW480 tumors, and both Western blot and immunohistochemistry analyses showed decreased NFκB (p65) expression in tumor tissues. Using TNF-α to induce NFκB activation in SW480 cells, it was revealed that C086 inhibited IκBα phosphorylation and its subsequent degradation, and suppressed the nuclear translocation and DNA binding activity of NFκB. C-Myc, cyclin D1, and Bcl-2, NFκB-regulated gene products involving in cellular proliferation a...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5219662</comments>
            <pubDate>Thu, 15 Sep 2011 09:16:11 +0100</pubDate>
            <guid isPermaLink="false">5219662</guid>        </item>
        <item>
            <title>Sorafenib attenuates p21 in kidney cancer cells and augments cell death in combination with DNA-damaging chemotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=5194734&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878748%26dopt%3DAbstract</link>
            <description>Authors: Inoue H, Hwang SH, Wecksler AT, Hammock BD, Weiss RH
    Abstract
    There are few effective therapeutic options for metastatic renal cell carcinoma (RCC). Conventional chemotherapeutic agents are ineffective since these tumors are unusually resistant to DNA damage, likely due to an exuberant DNA repair response. Sorafenib, as one of the few available effective therapeutic options for metastatic RCC, has been shown to inhibit cell proliferation by inhibition of tyrosine kinases. We have recently shown that sorafenib inhibits soluble epoxide hydrolase, which catalyzes metabolism of the anti-inflammatory epoxyeicosatrienoic acids. Given previous work demonstrating the anti-apoptotic role of p21 in RCC as a potential mechanism for its drug resistance, we asked whether sorafenib sign...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194734</comments>
            <pubDate>Mon, 05 Sep 2011 11:52:28 +0100</pubDate>
            <guid isPermaLink="false">5194734</guid>        </item>
        <item>
            <title>Synergistic efficacy of a novel combination therapy controls growth of Bcl-xL bountiful neuroblastoma cells by increasing differentiation and apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5194733&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878749%26dopt%3DAbstract</link>
            <description>In conclusion, our results appeared highly encouraging in advocating the use of 2,3-DCPE and 4-HPR as a novel combination therapy for increasing both differentiation and apoptosis in human malignant neuroblastoma cells having Bcl-xL overexpression.
    PMID: 21878749 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194733</comments>
            <pubDate>Mon, 05 Sep 2011 11:52:24 +0100</pubDate>
            <guid isPermaLink="false">5194733</guid>        </item>
        <item>
            <title>Development of a biomimetic peptide derived from collagen IV with anti-angiogenic activity in breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5194732&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21878750%26dopt%3DAbstract</link>
            <description>Authors: Rosca EV, Koskimaki JE, Pandey NB, Wolff AC, Popel AS
    Abstract
    Breast cancer is one of the most commonly diagnosed malignancies in women. Despite the remarkable success of mammography screening and use of adjuvant systemic therapy, it is estimated that approximately 200,000 new diagnoses will be made this year and 40,000 deaths will occur due to this disease (American Cancer Society). Angiogenesis, the growth of vessels from pre-existing microvasculature, is an essential component of tumor progression and has emerged as a therapeutic modality for anti-angiogenic therapies in cancer. Here we report in vitro and in vivo findings with a 20 amino acid peptide belonging to the collagen IV family, modified to facilitate possible translation to clinical applications. The two cyst...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194732</comments>
            <pubDate>Mon, 05 Sep 2011 11:52:19 +0100</pubDate>
            <guid isPermaLink="false">5194732</guid>        </item>
        <item>
            <title>Antibody microarray analysis of the serum proteome in primary breast cancer patients.</title>
            <link>http://www.medworm.com/index.php?rid=5194731&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885915%26dopt%3DAbstract</link>
            <description>Authors: Böhm D, Keller K, Boehm N, Lebrecht A, Schmidt M, Kölbl H, Grus FH
    Abstract
    Noninvasive biomarkers are urgently needed for detecting breast cancer as early as possible since the risk of recurrence, morbidity, and mortality is closely related to disease stage at the time of primary surgery. There are currently no such biomarkers in clinical use as a diagnostic tool. Proteomic analysis of protein expression patterns in body fluids has potential for use in identifying biomarkers of breast cancer. The aim of this study was to compare protein expression levels in the sera of primary breast cancer patients and healthy controls. An antibody microarray tool with 23 antibodies immobilized on nitrocellulose slides was used to determine the levels of acute phase proteins, interleuk...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194731</comments>
            <pubDate>Mon, 05 Sep 2011 11:52:15 +0100</pubDate>
            <guid isPermaLink="false">5194731</guid>        </item>
        <item>
            <title>VMY-1-103 is a novel CDK inhibitor that disrupts chromosome organization and delays metaphase progression in medulloblastoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=5194730&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885916%26dopt%3DAbstract</link>
            <description>Authors: Ringer L, Sirajuddin P, Heckler M, Ghosh A, Suprynowicz F, Yenugonda VM, Brown ML, Toretsky JA, Uren A, Lee Y, Macdonald TJ, Rodriguez O, Glazer RI, Schlegel R, Albanese C
    Abstract
    Medulloblastoma is the most prevalent of childhood brain malignancies, constituting 25% of childhood brain tumors. Craniospinal radiotherapy is a standard of care, followed by a 12-month regimen of multi-agent chemotherapy. For children less than 3 years of age, irradiation is avoided due to its destructive effects on the developing nervous system. Long-term prognosis is worst for these youngest children and more effective treatment strategies with a better therapeutic index are needed. VMY-1-103, a novel dansylated analog of purvalanol B, was previously shown to inhibit cell cycle progression a...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194730</comments>
            <pubDate>Mon, 05 Sep 2011 11:52:11 +0100</pubDate>
            <guid isPermaLink="false">5194730</guid>        </item>
        <item>
            <title>HO-3867, a curcumin analog, sensitizes cisplatin-resistant ovarian carcinoma, leading to therapeutic synergy through STAT3 inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=5194729&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21885917%26dopt%3DAbstract</link>
            <description>Authors: Selvendiran K, Ahmed S, Dayton A, Kuppusamy ML, Rivera BK, Kálai T, Hideg K, Kuppusamy P
    Abstract
    Cisplatin resistance is a major obstacle in the treatment of ovarian cancer. Drug combinations with synergistic or complementary functions are a promising strategy to overcome this issue. We studied the anticancer efficacy of a novel compound, HO-3867, used in combination with cisplatin against chemotherapy-resistant ovarian cancer. A2780R cells, a cisplatin-resistant human ovarian cancer cell line, were exposed to 1, 5, or 10 uM of HO-3867 alone or in combination with cisplatin (10 ug/ml) for 24 hours. Cell viability (MTT), proliferation (BrdU), cell-cycle analysis (FACS), and protein expression (western blot) were used for in vitro studies. STAT3 overexpression was performe...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5194729</comments>
            <pubDate>Mon, 05 Sep 2011 11:52:07 +0100</pubDate>
            <guid isPermaLink="false">5194729</guid>        </item>
        <item>
            <title>Hydrodynamic cell delivery for simultaneous establishment of tumor growth in mouse lung, liver and kidney.</title>
            <link>http://www.medworm.com/index.php?rid=5142013&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21832881%26dopt%3DAbstract</link>
            <description>Authors: Li J, Yao Q, Liu D
    Abstract
    To mimic advanced stage of cancer development involving multi-organ metastasis, hydrodynamic delivery commonly used in gene transfer was explored for establishing concurrent tumors in the lung, liver and kidney using B16-F1 melanoma cells, 4T1 breast cells and Renca renal carcinoma cells, as a model. The procedure involves a rapid injection into a mouse tail-vein of serum-free medium, containing tumor cells in a volume equal to approximately 7-9% of body weight. Compared to the conventional tail vein injection of tumor cells resulting in tumor growth only in the lung, hydrodynamic injection is highly effective in establishing tumor growth in the liver, kidney and lung. All tumor cells examined including melanoma, breast metastatic, and renal car...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142013</comments>
            <pubDate>Sat, 20 Aug 2011 04:08:06 +0100</pubDate>
            <guid isPermaLink="false">5142013</guid>        </item>
        <item>
            <title>Osteopontin increases breast cancer cell sensitivity to specific signaling pathway inhibitors in preclinical models.</title>
            <link>http://www.medworm.com/index.php?rid=5106596&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21795853%26dopt%3DAbstract</link>
            <description>This study used multiple in vitro assays to determine if OPN levels could predict breast cancer cell sensitivity to Hsp90 and/or Src kinase inhibitors. We used multiple derivatives of two unrelated of human breast cancer cell lines, high vs. low levels of OPN, to determine if OPN affects the response to two specific inhibitors, an Hsp90 inhibitor and a Src kinase inhibitor, in in vitro migration and colony formation assays. Cells had greater decreases in migration and colony forming ability after Hsp90 and Src kinase inhibitor treatments when OPN was present (either endogenous or exogenous). Decreasing OPN levels via shRNA knockdown decreased inhibitor effects. In rescue experiments, adding exogenous OPN to non-expressing cells increased inhibitor effects. These results suggest that OPN co...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106596</comments>
            <pubDate>Mon, 08 Aug 2011 22:19:28 +0100</pubDate>
            <guid isPermaLink="false">5106596</guid>        </item>
        <item>
            <title>Mitochondria-targeted nitroxides exacerbate Fluvastatin-mediated cytostatic and cytotoxic effects in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5106595&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21799303%26dopt%3DAbstract</link>
            <description>In this study, we investigated the antiproliferative and cytotoxic properties of submicromolar levels of Mito-CP11 alone and in combination with fluvastatin, a well known cholesterol lowering drug, in breast cancer cells. Mito-CP11, but not CP or CP plus the cationic ligand, methyl triphenylphosphonium (Me-TPP+), inhibited MCF-7 breast cancer cell proliferation. Mito-CP11 had only minimal effect on MCF-10A, non-tumorigenic mammary epithelial cells. Mito-CP11, however, significantly enhanced fluvastatin-mediated cytotoxicity in MCF-7 cells. Mito-CP11 alone and in combination with fluvastatin inhibited nuclear factor kappa-B activity mainly in MCF-7 cells. We conclude that mitochondria-targeted nitroxide antioxidant molecules (such as Mito-CP11) that are non-toxic to non-tumorigenic cells co...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106595</comments>
            <pubDate>Mon, 08 Aug 2011 22:18:59 +0100</pubDate>
            <guid isPermaLink="false">5106595</guid>        </item>
        <item>
            <title>Identification of tumorigenic cells and implication of their aberrant differentiation in human hemangioblastomas.</title>
            <link>http://www.medworm.com/index.php?rid=5106594&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811099%26dopt%3DAbstract</link>
            <description>Authors: Ma D, Zhu W, Zhang M, Ding X, Xu F, Hua W, Tang X, Zhu J, Mao Y, Zhou L
    The cytological origin of hemangioblastomas (HBs) is controversial possibly owing to limitation in the framework of normal vascular development. Our previous study reported that SSEA1 (stage-specific embryonic antigen-1) cells had the potential of HB-like structure formation in vitro cellular models. Here, we characterized primary proliferating tumor-initiating cells (TICs) and their neoplasmtic transformation. Neural stem cell marker SSEA1 and its lineage-related genes were demonstrated; no embryonic and mesenchymal stem cell markers were detected whereas their lineage-related genes in part were activated. Immunohistochemistry showed that the proliferating marker was preferentially expressed in SSEA1 cell...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106594</comments>
            <pubDate>Mon, 08 Aug 2011 22:18:24 +0100</pubDate>
            <guid isPermaLink="false">5106594</guid>        </item>
        <item>
            <title>Detection of apoptotic circulating tumor cells in advanced pancreatic cancer following 5-fluorouracil chemotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=5106593&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811100%26dopt%3DAbstract</link>
            <description>The objective of the present study was to evaluate CA19-9 and CK8/18 expression patterns in pancreatic cancer cell lines induced by 5-fluorouracil (5-Fu), and in circulating tumor cells (CTCs) in peripheral blood of patients previously untreated with advanced pancreatic cancer. Furthermore, the goal was to test the relationship of dynamic of CTCs with the effects of the first cycle of chemotherapy. To accomplish this study, CD45 antibody coated beads were used to discard white blood cells in peripheral blood. This was done in combination with CA19-9-Alexa488 and CK8/18-Alexa594 immunofluorescence staining to identify CTCs in circulation from 41 advanced pancreatic cancer patients, before and after chemotherapy. The PL45 pancreatic cancer cell line was incubated with 20 µmmol/L 5-Fu for 12...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106593</comments>
            <pubDate>Mon, 08 Aug 2011 22:17:52 +0100</pubDate>
            <guid isPermaLink="false">5106593</guid>        </item>
        <item>
            <title>Reexamining a proposal: Thymidylate synthase 5'-untranslated region as a regulator of translation efficiency.</title>
            <link>http://www.medworm.com/index.php?rid=5106592&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811101%26dopt%3DAbstract</link>
            <description>Authors: Ghosh S, Winter JM, Patel K, Kern SE
    The DNA replicative gene, thymidylate synthase (TYMS), is inhibited upon treatment with the anticancer drug 5-fluorouracil (5FU). TYMS has 28-bp tandem repeat sequences or VNTR (variable numbers of tandem repeats) in the 5'-untranslated region (5'-UTR). The number of these repeats is variable in any given population, but the most prevalent are double (2R) and triple (3R) repeat sequences. A single G/C nucleotide polymorphism in the triple repeat sequence gives rise to a 3Rc or a 3Rg triple repeat structure. A widely cited literature used plasmid constructs of the 5'-UTR and proposed that genotyping the TYMS UTRs would predict the efficiency of Tyms protein translation, justifying altered therapeutic dosage of 5FU. Prior studies had unusual ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106592</comments>
            <pubDate>Mon, 08 Aug 2011 22:17:21 +0100</pubDate>
            <guid isPermaLink="false">5106592</guid>        </item>
        <item>
            <title>Snail as a key regulator of PRL-3 gene in colorectal cancer.</title>
            <link>http://www.medworm.com/index.php?rid=5106591&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21811102%26dopt%3DAbstract</link>
            <description>Authors: Zheng P, Meng HM, Gao WZ, Chen L, Liu XH, Xiao ZQ, Liu YX, Sui HM, Zhou J, Liu YH, Li JM
    The regulators of a key metastasis gene PRL-3 in colorectal cancer (CRC) are still largely unknown. We found three potential binding sites of Snail, a key transcriptional factor involved in the epithelial-mesenchymal transition (EMT), in the region of PRL-3 promoter (located at -642 to -383). Moreover, our results showed that one of the Snail binding sites (located at -624 to -619) was the key element to maintain promoter activity of human PRL-3 gene. The transcriptional activity of PRL-3 promoter was abolished after the Snail binding site (located at -624 to -619) was mutated. Both promoter activity and protein expression of PRL-3 in CRC cell lines could be regulated by Snail. In clinical...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106591</comments>
            <pubDate>Mon, 08 Aug 2011 22:16:36 +0100</pubDate>
            <guid isPermaLink="false">5106591</guid>        </item>
        <item>
            <title>DNA mismatch repair proficiency executing 5-fluorouracil cytotoxicity in colorectal cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5106590&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21814034%26dopt%3DAbstract</link>
            <description>Conclusion: 5FdU as heteroduplex DNA in plasmid but not linear form triggered cytotoxicity in a MMR-dependent manner. Thus 5FU incorporated into DNA, separated from its effects on RNA, can be recognized by DNA MMR to trigger cell death.
    PMID: 21814034 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5106590</comments>
            <pubDate>Mon, 08 Aug 2011 22:16:03 +0100</pubDate>
            <guid isPermaLink="false">5106590</guid>        </item>
        <item>
            <title>Quantitative tissue proteomics of esophageal squamous cell carcinoma for novel biomarker discovery.</title>
            <link>http://www.medworm.com/index.php?rid=5059136&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743296%26dopt%3DAbstract</link>
            <description>In this study, our objective was to identify potential biomarkers for ESCC through a quantitative proteomic approach using the isobaric tags for relative and absolute quantitation (iTRAQ) approach. We compared the protein expression profiles of ESCC tumor tissues with the corresponding adjacent normal tissue from ten patients. LC-MS/MS analysis of strong cation exchange chromatography fractions was carried out on an Accurate Mass QTOF mass spectrometer, which led to the identification of 687 proteins. In all, 257 proteins were identified as differentially expressed in ESCC as compared to normal. We found several previously known protein biomarkers to be upregulated in ESCC including thrombospondin 1 (THBS1), periostin 1 (POSTN) and heat shock 70 kDa protein 9 (HSPA9) confirming the validit...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059136</comments>
            <pubDate>Mon, 25 Jul 2011 15:17:34 +0100</pubDate>
            <guid isPermaLink="false">5059136</guid>        </item>
        <item>
            <title>Hyperthermia increases the efficacy of survivinT34A against murine colon carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=5059135&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743297%26dopt%3DAbstract</link>
            <description>Authors: Li ZM, Zhao YW, Zhao CJ, Zhang XP, Chen LJ, Wei YO, Yang HS
    Survivin is a member of the inhibitor of apoptosis (IAP) family and plays an important role in inhibiting apoptosis and boosting angiogenesis, so targeting therapy of survivin is a promising strategy for advanced cancers. Similarly, hyperthermia is also a good approach to treat tumors in clinical. However, the improvement of antitumor efficacy is extremely limited for any single treatment. Here, we investigated the combined antitumor effect by using liposome-encapsulated mouse survivinT34A (mSurivinT34A) and hyperthermia on murine CT26 colon carcinoma. In our models, we found that the combination treatment of mSurivinT34A with hyperthermia significantly enhanced the apoptosis of CT26 cells and inhibited its growth in ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059135</comments>
            <pubDate>Mon, 25 Jul 2011 15:17:25 +0100</pubDate>
            <guid isPermaLink="false">5059135</guid>        </item>
        <item>
            <title>Anticancer biology of Azadirachta indica L (Neem): A mini review.</title>
            <link>http://www.medworm.com/index.php?rid=5059134&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743298%26dopt%3DAbstract</link>
            <description>Authors: Paul R, Prasad M, Sah NK
    Neem (Azadirachta indica), a member of the Meliaceae family, is a fast growing tropical evergreen tree with highly branched and stout solid stem. Because of its tremendous therapeutic, domestic, agricultural and ethnomedicinal significance, and proximity with human culture and civilization neem has been called as &quot;The Wonder Tree&quot; and &quot;Nature's Drug Store&quot;. All parts of this tree, particularly leaves, bark, seed-oil and their purified products are widely used for treatment of cancer. Over sixty different types of biochemicals including terpenoids and steroids have been purified from this plant. Pre-clinical research work done during the last decade has fine-tuned our understanding of the anti-cancer properties of the crude and purified products from th...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059134</comments>
            <pubDate>Mon, 25 Jul 2011 15:17:16 +0100</pubDate>
            <guid isPermaLink="false">5059134</guid>        </item>
        <item>
            <title>MicroRNA-34a targets notch1 and inhibits cell proliferation in glioblastoma multiforme.</title>
            <link>http://www.medworm.com/index.php?rid=5059133&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21743299%26dopt%3DAbstract</link>
            <description>In this study, we found that microRNA-34a (miR-34a) is significantly downregulated in glioblastoma multiforme (GBM) specimens compared with normal brain tissues. Growth curve and colony formation assays revealed that miR-34a suppresses proliferation of U373MG and SHG44 glioblastoma cells. Overexpression of miR-34a could induce apoptosis of glioblastoma cells. Also, we identified notch1 as a direct target gene of miR-34a. Knockdown of notch1 showed similar cellular functions as overexpression of miR-34a both in vitro and in vivo. Collectively, our findings show that miR-34a is downregulated in GBM cells and inhibits GBM growth by targeting notch1.
    PMID: 21743299 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059133</comments>
            <pubDate>Mon, 25 Jul 2011 15:17:07 +0100</pubDate>
            <guid isPermaLink="false">5059133</guid>        </item>
        <item>
            <title>Frequent detection of infectious xenotropic murine leukemia virus (XMLV) in human cultures established from mouse xenografts.</title>
            <link>http://www.medworm.com/index.php?rid=5059132&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750403%26dopt%3DAbstract</link>
            <description>Conclusions: Human cultures derived after mouse xenografting frequently contain and release highly infectious xenotropic MLV viruses. Laboratories working with xenograft-derived human cultures should be aware of the risk of contamination with potentially biohazardous human-tropic mouse viruses and their horizontal spread to other cultures.
    PMID: 21750403 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059132</comments>
            <pubDate>Mon, 25 Jul 2011 15:16:56 +0100</pubDate>
            <guid isPermaLink="false">5059132</guid>        </item>
        <item>
            <title>Oncogenic roles of astrocyte elevated gene-1 (AEG-1) in osteosarcoma progression and prognosis.</title>
            <link>http://www.medworm.com/index.php?rid=5059131&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21750404%26dopt%3DAbstract</link>
            <description>Authors: Wang F, Ke ZF, Sun SJ, Chen WF, Yang SC, Li SH, Mao XP, Wang LT
    Astrocyte elevated gene-1 (AEG-1) is overexpressed in several cancers and plays an important role in cancer progression. However, AEG-1 expression, biological function, and clinical significance in osteosarcoma have not been uncovered. Utilizing manipulated human osteosarcoma cell lines and osteosarcoma tissues, we found that increasing expression of AEG-1 enhanced osteosarcoma cell proliferation and invasion in vitro, and knockdown of AEG-1 significantly attenuated osteosarcoma cell malignancy. Moreover, AEG-1 was overexpressed in osteosarcoma tissues, and overexpression of AEG-1 was strongly associated with gender (p = 0.018), clinical stages (p &amp;lt; 0.001), classification (p &amp;lt; 0.001), metastasis (p = 0.013),...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059131</comments>
            <pubDate>Mon, 25 Jul 2011 15:16:47 +0100</pubDate>
            <guid isPermaLink="false">5059131</guid>        </item>
        <item>
            <title>Spectral imaging-based methods for quantifying autophagy and apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5059130&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21757995%26dopt%3DAbstract</link>
            <description>In this study we coupled spectral imaging with fluorescence and white light microscopy to develop new methods for quantifying autophagy and apoptosis. For autophagy, we employed multispectral imaging to examine spectral changes in the fluorescence of LC3-GFP, a chimeric protein commonly used to track autophagosome formation. We found that punctate autophagosome-associated LC3-GFP exhibited a spectral profile that was distinctly different from diffuse cytosolic LC3-GFP. We then exploited this shift in spectral quality to quantify the amount of autophagosome-associated signal in single cells. Hydroxychloroquine (CQ), an anti-malarial agent that increases autophagosomal number, significantly increased the punctate LC3-GFP spectral signature, providing proof-of-principle for this approach. For...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059130</comments>
            <pubDate>Mon, 25 Jul 2011 15:16:36 +0100</pubDate>
            <guid isPermaLink="false">5059130</guid>        </item>
        <item>
            <title>Vinblastine sensitizes leukemia cells to cyclin-dependent kinase inhibitors, inducing acute, cell cycle phase-independent apoptosis.</title>
            <link>http://www.medworm.com/index.php?rid=5059123&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21768777%26dopt%3DAbstract</link>
            <description>Authors: Bates DJ, Salerni BL, Lowrey CH, Eastman A
    The efficacy of many chemotherapeutic agents can be attenuated by expression of the anti-apoptotic proteins Bcl-2, Bcl-XL and Mcl-1. Flavopiridol and dinaciclib are cyclin-dependent kinase 7 and 9 inhibitors that transcriptionally inhibit expression of Mcl-1. We have investigated the ability of flavopiridol and dinaciclib to sensitize a panel of leukemia cell lines to vinblastine and paclitaxel. Both drugs acutely sensitized most of the leukemia lines to vinblastine, with 100% apoptosis in 4 h. Furthermore, dinaciclib sensitized freshly isolated chronic lymphocytic leukemia cells to vinblastine. This rapid induction of apoptosis was attributed to vinblastine-mediated activation of JNK because (a) flavopiridol and dinaciclib failed to ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059123</comments>
            <pubDate>Mon, 25 Jul 2011 15:16:23 +0100</pubDate>
            <guid isPermaLink="false">5059123</guid>        </item>
        <item>
            <title>Hyperspectral imaging: A non-invasive method of imaging melanoma lesions in a patient with stage IV melanoma, being treated with a RAF inhibitor.</title>
            <link>http://www.medworm.com/index.php?rid=5059117&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21768778%26dopt%3DAbstract</link>
            <description>Authors: Dicker DT, Kahn N, Flaherty KT, Lerner J, El-Deiry WS
    Utilizing a macroscopic Prism and Reflectance Imaging Spectroscopy System (MACRO-PARISS), spectral data are taken from human skin using a fiber optic light probe. The subject was an oncology patient at the University of Pennsylvania, with biopsy proven melanoma, who underwent chemotherapy with a novel small molecule BRAF inhibitor as part of a Phase I clinical trial. The BRAF mutation had been previously identified in this patient. Cutaneous lesions were identified by a clinical oncologist, and lesions were imaged periodically over a 1 month period of time. Spectra are classified using a linearity-independent algorithm over a wavelength range of 450-920 nm. Spectral signatures, or characteristic features, of generated spect...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059117</comments>
            <pubDate>Mon, 25 Jul 2011 15:16:12 +0100</pubDate>
            <guid isPermaLink="false">5059117</guid>        </item>
        <item>
            <title>Cyclin-dependent kinase inhibitor Dinaciclib (SCH727965) inhibits pancreatic cancer growth and progression in murine xenograft models.</title>
            <link>http://www.medworm.com/index.php?rid=5059116&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21768779%26dopt%3DAbstract</link>
            <description>Authors: Feldmann G, Mishra A, Bisht S, Karikari C, Garrrido-Laguna I, Rasheed Z, Ottenhof N, Dadon T, Alvarez H, Fendrich V, Rajeshkumar NV, Matsui W, Brossart P, Hidalgo M, Bannerji R, Maitra A, Nelkin BD
    Pancreatic cancer is one of the most lethal of human malignancies, and potent therapeutic options are lacking. Inhibition of cell cycle progression through pharmacological blockade of cyclin-dependent kinases (CDK) has been suggested as a potential treatment option for human cancers with deregulated cell cycle control. Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials. I...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059116</comments>
            <pubDate>Mon, 25 Jul 2011 15:16:00 +0100</pubDate>
            <guid isPermaLink="false">5059116</guid>        </item>
        <item>
            <title>Atorvastatin induces autophagy in prostate cancer PC3 cells through activation of LC3 transcription.</title>
            <link>http://www.medworm.com/index.php?rid=5059115&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21768780%26dopt%3DAbstract</link>
            <description>This study attempts to elucidate the molecular mechanism underlying atorvastatin-induced autophagy in PC3 cells. PC3 cells were treated with atorvastatin, in combination with the inhibitors for transcription, protein translation, PI-3 kinase, mTOR, and MAP kinases. The atorvastatin-induced elevation of LC3-II was inhibited by both the translational and the transcriptional inhibitors, suggesting that the inhibition of geranylgeranyl biosynthesis by atorvastatin activates transcription of LC3, which results in elevation of LC3-II and activation of autophagy. RT-PCR and quantitative PCR assays showed that atorvastatin enhanced expression of LC3 mRNA, and addition of geranylgeraniol along with atorvastatin to the medium eliminated the enhancement, confirming the activation of transcription of ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059115</comments>
            <pubDate>Mon, 25 Jul 2011 15:15:48 +0100</pubDate>
            <guid isPermaLink="false">5059115</guid>        </item>
        <item>
            <title>Anticancer imidazoacridinone C-1311 inhibits hypoxia-inducible factor-1 alpha (HIF-1α), vascular endothelial growth factor (VEGF) and angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5059111&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21775820%26dopt%3DAbstract</link>
            <description>Authors: Paradziej-Lukowicz J, Skwarska A, Peszyńska-Sularz G, Brillowska-Dąbrowska A, Konopa J
    Antitumor imidazoacridinone C-1311 is a DNA-reactive topoisomerase II and FLT3 receptor tyrosine kinase inhibitor. Here, we demonstrate the mechanism of C-1311 inhibitory action on novel targets: hypoxia-inducible factor-1α (HIF-1α), vascular-endothelial growth factor (VEGF), and angiogenesis. In a cell-free system, C-1311 prevented HIF-1α binding to an oligonucleotide encompassing a canonical hypoxia-responsive element (HRE), but did not directly interfere with HIF-1α protein. Whereas C-1311 did not affect HIF-1α transcription, at higher concentrations (10 µM), it decreased HIF-1α protein accumulation. Furthermore, C-1311 potently reduced the transcription of HIF-1-dependent report...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059111</comments>
            <pubDate>Mon, 25 Jul 2011 15:15:37 +0100</pubDate>
            <guid isPermaLink="false">5059111</guid>        </item>
        <item>
            <title>Increased migration of a human glioma cell line after in vitro Cyberknife irradiation.</title>
            <link>http://www.medworm.com/index.php?rid=5059099&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21775821%26dopt%3DAbstract</link>
            <description>Authors: Canazza A, Calatozzolo C, Fumagalli L, Bergantin A, Ghielmetti F, Fariselli L, Croci D, Salmaggi A, Ciusani E
    A human glioblastoma multiforme cell line (U87) and its derived-spheroids were irradiated either using a conventional irradiation (CIR) or a CK-like irradiation (IIR) in which the 8Gy was delivered intermittently over a period of 40 minutes. The ability of glioma cells to migrate into a matrigel matrix was evaluated on days 1-8 from irradiation. Irradiation with CK-driven IIR significantly increased the invasion potential of U87 cells in a matrigel-based assay. In contrast to CIR, IIR was associated with increased levels of TGF-B at four days (Real time PCR), β1-integrin at 4-5 days (real-time PCR and western blot) and no elevation in phosphorylated AKT at days 4 and ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059099</comments>
            <pubDate>Mon, 25 Jul 2011 15:15:27 +0100</pubDate>
            <guid isPermaLink="false">5059099</guid>        </item>
        <item>
            <title>Src family kinases mediate epidermal growth factor receptor signaling from lipid rafts in breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=5059093&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21775822%26dopt%3DAbstract</link>
            <description>Authors: Irwin ME, Bohin N, Boerner J
    Activation of the epidermal growth factor receptor (EGFR) regulates cellular proliferation, survival, and migration of breast cancer cells. In particular, EGFR recruits signaling proteins to the cell membrane leading to their phosphorylation and activation. However, EGFR also localizes to other cellular structures, including endosomes, mitochondrion, and nuclei. Recently, we demonstrated that lipid raft localization of EGFR in triple-negative breast cancer cell lines promotes EGFR protein-dependent, EGFR kinase-independent activation of Akt. Here, we further define the mechanism by which lipid rafts regulate EGFR signaling to Akt. Specifically, we show that the non-receptor tyrosine kinase c-Src co-localizes and co-associates with EGFR and lipid ra...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5059093</comments>
            <pubDate>Mon, 25 Jul 2011 15:15:16 +0100</pubDate>
            <guid isPermaLink="false">5059093</guid>        </item>
        <item>
            <title>Augmentation of NVP-BEZ235&amp;#39;s anticancer activity against human lung cancer cells by blockage of autophagy.</title>
            <link>http://www.medworm.com/index.php?rid=5011326&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21738008%26dopt%3DAbstract</link>
            <description>Authors: Xu CX, Zhao L, Yue P, Fang G, Tao H, Owonikoko TK, Ramalingam SS, Khuri FR, Sun SY
    Autophagy is a cellular lysosomal degradation pathway essential for regulation of cell survival and death to maintain homeostasis. This process is negatively regulated by mammalian target of rapamycin (mTOR) signaling and often counteracts efficacy of certain cancer therapeutic agents. NVP-BEZ235 (BEZ235) is a novel, orally bioavailable dual PI3K/mTOR inhibitor that has exhibited promising activity against non-small cell lung cancer (NSCLC) in preclinical models. The current study focuses on evaluating the role of BEZ235 in regulating autophagy. BEZ235 was effective in inhibiting the growth of NSCLC cells including induction of apoptosis. It also potently induced the expression of type-II LC3, i...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5011326</comments>
            <pubDate>Mon, 11 Jul 2011 00:33:43 +0100</pubDate>
            <guid isPermaLink="false">5011326</guid>        </item>
        <item>
            <title>Identification and gene expression profiling of tumor-initiating cells isolated from human osteosarcoma cell lines in an orthotopic mouse model.</title>
            <link>http://www.medworm.com/index.php?rid=4921043&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21617384%26dopt%3DAbstract</link>
            <description>Authors: Rainusso N, Man TK, Lau CC, Hicks J, Shen JJ, Yu A, Wang LL, Rosen JM
    In the cancer stem cell model a cell hierarchy has been suggested as an explanation for intratumoral heterogeneity and tumor formation is thought to be driven by this tumor cell subpopulation. The identification of cancer stem cells in osteosarcoma (OS) and the biological processes dysregulated in this cell subpopulation, also known as tumor-initiating cells (TICs), may provide new therapeutic targets. The goal of this study, therefore, was to identify and characterize the gene expression profiles of TICs isolated from human OS cell lines. We analyzed the self-renewal capacity of OS cell lines and primary OS tumors based upon their ability to form sphere-like structures (sarcospheres) under serum-starving co...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4921043</comments>
            <pubDate>Sat, 11 Jun 2011 10:45:17 +0100</pubDate>
            <guid isPermaLink="false">4921043</guid>        </item>
        <item>
            <title>Inhibition of N-myc downstream-regulated gene 2 In prostatic carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4921042&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21623166%26dopt%3DAbstract</link>
            <description>Authors: Yu C, Wu G, Dang N, Zhang W, Zhang R, Yan W, Zhao Y, Gao L, Wang Y, Beckwith N, Yuan J, Yao L
    To study the expression of N-myc Downstream Regulated Gene-2 (NDRG2) in prostatic carcinoma (PCA) tissue and in different PCA cell lines, and to investigate its clinical and pathological implications, 144 PCA and benign prostatic hyperplasia (BPH) tissue sections were analyzed retrospectively with immunohistochemistry (S-P method). The expression levels of NDRG2 and c-Myc in prostate cell lines were detected through Western blot. The effects of adenovirus-mediated NDRG2 on PC3 cells and PC3 nude mouse xenografts was observed through cell growth curves, tumor growth curves, flow cytometry (FCM), transmission electron microscopy (TEM) and TUNEL staining. The NDRG2 gene was highly expres...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4921042</comments>
            <pubDate>Sat, 11 Jun 2011 10:45:13 +0100</pubDate>
            <guid isPermaLink="false">4921042</guid>        </item>
        <item>
            <title>Src family kinases and paclitaxel sensitivity.</title>
            <link>http://www.medworm.com/index.php?rid=4921041&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21646863%26dopt%3DAbstract</link>
            <description>Authors: Le XF, Bast RC
    Src-family Kinases (SFKs) participate in the regulation of proliferation, differentiation, apoptosis, autophagy, adhesion, migration, invasion and angiogenesis in normal and cancer cells. Abnormal expression of SFKs has been documented in cancers that arise in breast, colon, ovary, melanocyte, gastric mucosa, head and neck, pancreas, lung, and brain. Targeting SFKs in cancer cells has been shown to be a promising therapeutic strategy in solid tumors, particularly in ovarian, colon and breast cancers. Paclitaxel is one of most widely used chemotherapeutic agents for the management of ovarian, breast, lung and head/neck cancers. As a microtubule-stabilizing agent, paclitaxel possesses both mitosis-dependent and mitosis-independent activities against cancer cells. ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4921041</comments>
            <pubDate>Sat, 11 Jun 2011 10:45:08 +0100</pubDate>
            <guid isPermaLink="false">4921041</guid>        </item>
        <item>
            <title>Systemic Par-4 inhibits non-autochthonous tumor growth.</title>
            <link>http://www.medworm.com/index.php?rid=4872578&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613819%26dopt%3DAbstract</link>
            <description>Authors: Zhao Y, Burikhanov R, Brandon J, Qiu S, Shelton BJ, Spear B, Bondada S, Bryson S, Rangnekar VM
    The tumor suppressor protein Par-4 (Prostate apoptosis response-4) is spontaneously secreted by normal and cancer cells. Extracellular Par-4 induces caspase-dependent apoptosis in cancer cell cultures by binding, via its effector SAC domain, to cell surface GRP78 receptor. However, the functional significance of extracellular Par-4/SAC has not been validated in animal models. We show that Par-4/SAC-transgenic mice express systemic Par-4/SAC protein and are resistant to the growth of non-autochthonous tumors. Consistently, secretory Par-4/SAC pro-apoptotic activity can be transferred from these cancer-resistant transgenic mice to cancer-susceptible mice by bone marrow transplantation....</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872578</comments>
            <pubDate>Sat, 28 May 2011 06:46:05 +0100</pubDate>
            <guid isPermaLink="false">4872578</guid>        </item>
        <item>
            <title>Cancer-testis gene expression profiling in esophageal squamous cell carcinoma: Identification of specific tumor marker and potential targets for immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=4872577&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613820%26dopt%3DAbstract</link>
            <description>Authors: Forghanifard MM, Gholamin M, Farshchian M, Moaven O, Memar B, Forghani MN, Dadkhah E, Naseh H, Moghbeli M, Raeisossadati R, Abbaszadegan MR
    Cancer-testis antigens (CTAs) are often specifically expressed in cancer cells and under normal conditions are only considered to be expressed in the germ line cells and the placenta. CTAs are potential targets for cancer immunotherapy and therefore necessitates their expression profiling. The expression profile of LAGE1, MAGE-A4 and NY-ESO1, their possible correlations and interaction, and the clinicopathological associations of each marker were studied. RNA was extracted from fresh esophagectomy tissues of 41 esophageal squamous cell carcinoma (ESCC) patients prior to any other therapeutic intervention. The relative mRNA expression of LA...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872577</comments>
            <pubDate>Sat, 28 May 2011 06:46:01 +0100</pubDate>
            <guid isPermaLink="false">4872577</guid>        </item>
        <item>
            <title>Complete remission, in BRCA2 mutation carrier with metastatic pancreatic adenocarcinoma, treated with cisplatin based therapy.</title>
            <link>http://www.medworm.com/index.php?rid=4872576&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613821%26dopt%3DAbstract</link>
            <description>In conclusion, in patients with known BRCA mutation associated pancreatic adenocarcinoma, the addition of a DNA cross-linking agent such as cisplatin should be considered. Physicians should consider BRCA mutation testing when the diagnosis of pancreatic cancer is established, especially when the patient belongs to an ethnic group where founder mutations exist, and/or there is strong personal or family history of cancer. This may be applied also to other metastatic tumors diagnosed in BRCA1/2 carriers.
    PMID: 21613821 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872576</comments>
            <pubDate>Sat, 28 May 2011 06:45:57 +0100</pubDate>
            <guid isPermaLink="false">4872576</guid>        </item>
        <item>
            <title>A novel three-dimensional culture system uncovers growth stimulatory actions by TGF-β in pancreatic cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4872575&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613822%26dopt%3DAbstract</link>
            <description>Authors: Sempere LF, Gunn JR, Korc M
    Transforming Growth Factor-β (TGF-β) exerts cell type-specific and context-dependent effects. Understanding the intrinsic effects of TGF-β on cancer cells in pancreatic ductal adenocarcinoma (PDAC) is a prerequisite for rationalized clinical implementation of TGF-β targeting therapies. Since the tumor microenvironment can affect how cancer cell respond to TGF-β, we employed a novel three-dimensional (3D) culturing system to recapitulate stromal and extracellular matrix interactions. We show here that TGF-β stimulates growth of human and murine pancreatic cancer cell lines (PCCs) when embedded in a 3% collagen IV/laminin-rich gelatinous medium (MatrigelÔ) over a solidified layer of soft agar. Moreover, in this novel 3D model, concomitant treat...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872575</comments>
            <pubDate>Sat, 28 May 2011 06:45:54 +0100</pubDate>
            <guid isPermaLink="false">4872575</guid>        </item>
        <item>
            <title>Troglitazone, a PPAR agonist, inhibits human prostate cancer cell growth through inactivation of NF-kB via suppression of GSK-3β expression.</title>
            <link>http://www.medworm.com/index.php?rid=4872574&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613824%26dopt%3DAbstract</link>
            <description>Authors: Ban JO, Oh JH, Son SM, Won D, Song HS, Han SB, Moon DC, Kang KW, Song MJ, Hong JT
    PPARγ ligands have been reported to reduce proliferation of human prostate cancer cells. However, the molecular mechanism of PPARγagonist-induced cell growth inhibition of prostate cancer cells is not clear. GSK-3b expression and NF-kB activity have important roles in prostate cancer development. To investigate the mechanisms of the PPARγagonist-induced prostate cancer cell growth inhibition, we examined the effect of troglitazone on the expression of PPARγ, GSK-3band activity of NF-kB as well as on the prostate cancer cell growth. Troglitazone induced the expression of PPARγ in the nuclear of PC-3 cells, but not in LNCaP cells. Troglitazone (0-16 uM) inhibited cancer cell growth in...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872574</comments>
            <pubDate>Sat, 28 May 2011 06:45:49 +0100</pubDate>
            <guid isPermaLink="false">4872574</guid>        </item>
        <item>
            <title>FoxO family members in cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4872573&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613825%26dopt%3DAbstract</link>
            <description>Authors: Zhang Y, Gan B, Paik JH
    The PI3K-Akt-FoxO signaling pathway plays a central role in diverse physiological processes including cellular energy storage, growth, and survival, among others. As an important effector of this pathway, FoxO is involved in versatile activities that protect organisms from stress and aging. Recent studies on mammalian FoxO have established a direct role for this transcription factor family in cellular proliferation, oxidative stress response, and tumorigenesis. The review will focus on the recent developments pertaining to the function of FoxO as well as discuss the various contexts in which FoxO exerts distinct biological activity such as drug resistance and autophagy in cancer pathogenesis and therapy.
    PMID: 21613825 [PubMed - as supplied by publi...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872573</comments>
            <pubDate>Sat, 28 May 2011 06:45:44 +0100</pubDate>
            <guid isPermaLink="false">4872573</guid>        </item>
        <item>
            <title>Decreased zinc and down regulation of ZIP3 zinc uptake transporter in the development of pancreatic adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4872572&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613827%26dopt%3DAbstract</link>
            <description>This report provides the clinical foundation for further mechanistic studies that will provide important insight into pancreatic carcinogenesis, and can lead to the development of effective early biomarkers and effective therapeutic agents for pancreatic cancer.
    PMID: 21613827 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872572</comments>
            <pubDate>Sat, 28 May 2011 06:45:21 +0100</pubDate>
            <guid isPermaLink="false">4872572</guid>        </item>
        <item>
            <title>Combination of ultrasound and Bubble liposome enhance the effect of doxorubicin and inhibit murine osteosarcoma growth.</title>
            <link>http://www.medworm.com/index.php?rid=4872571&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21613828%26dopt%3DAbstract</link>
            <description>Authors: Ueno Y, Sonoda S, Suzuki R, Yokouchi M, Kawasoe Y, Tachibana K, Maruyama K, Sakamoto T, Komiya S
    If ultrasound (US) is applied to cells, permeability across the cell membrane temporarily increases, making it easier for drugs to be taken into the cells from around the cell membrane. Moreover, when used in combination with Bubble liposome (BL: liposomes which entrap an ultrasound imaging gas), even low-power ultrasound can facilitate drug delivery into cells. In the present study, we constructed a new drug delivery system (DDS) involving concomitant use of US and BL with doxorubicin (DOX), a key drug in the chemotherapy of osteosarcoma, and demonstrated both in vitro and in vivo that it markedly inhibited the proliferation of osteosarcoma cells. Furthermore, this system achieved...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4872571</comments>
            <pubDate>Sat, 28 May 2011 06:45:13 +0100</pubDate>
            <guid isPermaLink="false">4872571</guid>        </item>
        <item>
            <title>Autophagy inhibition cooperates with erlotinib to induce glioblastoma cell death.</title>
            <link>http://www.medworm.com/index.php?rid=4818049&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21508666%26dopt%3DAbstract</link>
            <description>Authors: Eimer S, Belaud-Rotureau MA, Airiau K, Jeanneteau M, Laharanne E, Véron N, Vital A, Loiseau H, Merlio JP, Belloc F
    Gliomas are the most common malignant primary brain tumors in adults. The median survival never exceeds 12 months, owing to inherent resistance to both radio and chemotherapies. Epidermal Growth Factor Receptor (EGFR) is amplified, overexpressed, and/or mutated in glioblastomas (GBM), making it a rational for therapy. Erlotinib, an EGFR kinase inhibitor is strongly associated with clinical response in several cancers. Inhibition of cell proliferation and induction of apoptosis by erlotinib were investigated in U87-MG and DBTRG-05MG, two human glioblastoma cell lines. The expression of several apoptosis-related proteins was investigated in these cell lines and in ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818049</comments>
            <pubDate>Fri, 13 May 2011 17:02:06 +0100</pubDate>
            <guid isPermaLink="false">4818049</guid>        </item>
        <item>
            <title>Role of GPER/GPR30 in tumoral testicular germ cells proliferation.</title>
            <link>http://www.medworm.com/index.php?rid=4818048&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21508670%26dopt%3DAbstract</link>
            <description>Authors: Chevalier N, Bouskine A, Fenichel P
    In a recent issue of Cancer Biology &amp; Therapy, Vitale et al. introduced the paper of Franco et al. reporting the expression of GPER (a seven-transmembrane-spanning receptor also known as GPR30) on testicular germ cell tumors (TGCTs). The paper commented on the possible pathophysiological role of this G-protein-coupled receptor (GPCR) during testicular germ cell carcinogenesis. They also proposed the potential use of selective antagonists of GPER as new-targeted therapy in these tumors. We agree with this hypothesis and would like to highlight here some published results supporting this hypothesis and give some details concerning the role of estrogens and xeno-estrogens in testicular carcinogenesis and the effects of GPER antagonist in hu...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818048</comments>
            <pubDate>Fri, 13 May 2011 17:02:02 +0100</pubDate>
            <guid isPermaLink="false">4818048</guid>        </item>
        <item>
            <title>Oral ingestion of Streptococcus thermophilus does not affect mucositis severity or tumor progression in the tumor-bearing rat.</title>
            <link>http://www.medworm.com/index.php?rid=4818047&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21508671%26dopt%3DAbstract</link>
            <description>Authors: Tooley KL, Howarth GS, Lymn KA, Lawrence A, Butler RN
    Preventative or adjunctive agents for the amelioration of small intestinal chemotherapy-induced mucositis are not currently available for clinical use. We have previously demonstrated that oral ingestion of Streptococcus thermophilus (TH-4) partially attenuated chemotherapy-induced mucositis in the rat. Here we assess the effects of TH-4 on small intestinal damage and tumor progression in tumor-bearing rats with experimentally-induced mucositis. Female Dark Agouti tumor-bearing (mammary adenocarcinoma) rats (n = 36; 139 ± 1 g) had small intestinal damage induced via the administration of methotrexate (MTX). Rats were administered MTX; (1.5 mg/kg intramuscular) or saline at 0 and 24 h; with daily gavage administration of TH...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818047</comments>
            <pubDate>Fri, 13 May 2011 17:01:58 +0100</pubDate>
            <guid isPermaLink="false">4818047</guid>        </item>
        <item>
            <title>Targeting inhibitor of apoptosis proteins in combination with dacarbazine or TRAIL in melanoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4818046&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21508672%26dopt%3DAbstract</link>
            <description>We examined the importance of the IAPs in the resistance to the commonly used chemotherapeutic agent dacarbazine (DTIC) and the apoptosis inducer TRAIL (TNF-related apoptosis inducing ligand) in malignant melanoma. The data presented show that the expression of IAPs is universal, concomitant and generally high in melanoma cell lines and in patient samples. Depleting IAP expression by siRNA tended to reduce cell viability, with XIAP reduction being the most efficient in all four cell lines examined (FEMX-1, LOX, SKMEL-28 and WM115). The combined treatment of XIAP siRNA and DTIC showed a weak improvement in two of four cell lines, while all four cell lines showed enhanced sensitivity towards TRAIL (AdhCMV-TRAIL) after XIAP depletion. In addition, cIAP-1, cIAP-2 and survivin down-regulation s...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818046</comments>
            <pubDate>Fri, 13 May 2011 17:01:54 +0100</pubDate>
            <guid isPermaLink="false">4818046</guid>        </item>
        <item>
            <title>Phase II trial of bevacizumab and dose/dense chemotherapy with cisplatin and metronomic daily oral etoposide in advanced non-small-cell-lung cancer patients.</title>
            <link>http://www.medworm.com/index.php?rid=4818045&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21525780%26dopt%3DAbstract</link>
            <description>Authors: Correale P, Botta C, Basile A, Pagliuchi M, Licchetta A, Martellucci I, Bestoso E, Apollinari S, Addeo R, Misso G, Romano O, Abbruzzese A, Lamberti M, Luzzi L, Gotti G, Rotundo MS, Caraglia M, Tagliaferri P
    Bevacizumab, is a humanized monoclonal antibody to vasculo-endothelial-growth-factor, with anti-cancer activity in non-small-cell-lung cancer (NSCLC) patients. Our previous results from a dose/finding phase I trial in NSCLC patients, demonstrated the anti-angiogenic effects and toxicity of a newest bevacizumab-based combination with fractioned cisplatin and daily oral etoposide. We designed a phase II trial to evaluate in advanced NSCLC patients the antitumor activity and the safety of this novel regimen. In particular, 45 patients (36 males and 9 females), with a mean age ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818045</comments>
            <pubDate>Fri, 13 May 2011 17:01:49 +0100</pubDate>
            <guid isPermaLink="false">4818045</guid>        </item>
        <item>
            <title>Chemoresponse assay for evaluating response to sunitinib in primary cultures of breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4818044&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21525781%26dopt%3DAbstract</link>
            <description>Conclusions: Chemoresponse assay assessment is an effective tool for evaluating sunitinib sensitivity in cultured cell lines as well as ex vivo breast cancer samples. An in vitro assay that may indicate an individual patient's clinical response to a chemotherapeutic agent can be beneficial in time, cost, and clinical outcome when therapeutic options are considered.
    PMID: 21525781 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818044</comments>
            <pubDate>Fri, 13 May 2011 17:01:38 +0100</pubDate>
            <guid isPermaLink="false">4818044</guid>        </item>
        <item>
            <title>Troglitazone suppresses c-Myc levels in human prostate cancer cells via a PPARγ-independent mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=4818043&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21525782%26dopt%3DAbstract</link>
            <description>Authors: Akinyeke TO, Stewart LV
    Troglitazone is a ligand for the peroxisome proliferator activated receptor gamma (PPARγ) that decreases growth of human prostate cancer cells in vitro and in vivo. However, the mechanism by which troglitazone reduces prostate cancer cell growth is not fully understood. To understand the signaling pathways involved in troglitazone-induced decreases in prostate cancer growth, we examined the effect of troglitazone on androgen-independent C4-2 human prostate cancer cells. Initial experiments revealed troglitazone inhibited C4-2 cell proliferation by arresting cells in the G0/G1 phase of the cell cycle and inducing apoptosis. Since the proto-oncogene product c-Myc regulates both apoptosis and cell cycle progression, we next examined whether troglitazone a...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818043</comments>
            <pubDate>Fri, 13 May 2011 17:01:28 +0100</pubDate>
            <guid isPermaLink="false">4818043</guid>        </item>
        <item>
            <title>The insulin-like growth factor binding proteins 3 and 7 are associated with colorectal cancer and liver metastasis.</title>
            <link>http://www.medworm.com/index.php?rid=4818042&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21525788%26dopt%3DAbstract</link>
            <description>In this study, we intended to shed more light on two essential members; IGFBP3 as representative for the six main IGFBPs and IGFBP7 to represent their related proteins (IGFBP-rps). Our experiments on silencing IGFBP3 or IGFBP7 in the two human CRC cell lines SW480, Caco2, and in the rat CRC cell line CC531 show reduced proliferation, colony formation, and for IGFBP3, also reduced migration. The expression of both genes in 68 human CRC samples was higher in UICC stages II and III than in stages I and IV. Additionally, IGFBP3 was negatively correlated with age (p = 0.05) and positively related to IGFBP7 expression (p = 0.0001). Further, in a liver metastasis experiment, the expression of both genes was drastically increased in response to early metastatic growth in vivo. Since these high lev...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818042</comments>
            <pubDate>Fri, 13 May 2011 17:01:22 +0100</pubDate>
            <guid isPermaLink="false">4818042</guid>        </item>
        <item>
            <title>TOFA (5-tetradecyl-oxy-2-furoic acid) reduces fatty acid synthesis, inhibits expression of AR, neuropilin-1, and Mcl-1 and kills prostate cancer cells independent of p53 status.</title>
            <link>http://www.medworm.com/index.php?rid=4818041&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21525791%26dopt%3DAbstract</link>
            <description>Authors: Guseva NV, Rokhlin OW, Glover RA, Cohen MB
    A key player in prostate cancer development and progression is the androgen receptor (AR). Tumor-associated lipogenesis can protect cancer cells from carcinogenic- and therapeutic-associated treatments. Increased synthesis of fatty acids and cholesterol is regulated by androgens through induction of several genes in androgen-responsive cancer cells. Acetyl-CoA-carboxylase-α (ACCA) is a key enzyme in the regulation of fatty acids synthesis. Here we show that AR binds in vivo to intron regions of human ACCA gene. We also show that the level of ACCA protein in LNCaP depends on AR expression and that DHT treatment increases ACCA expression and fatty acid synthesis. Inhibition of ACCA by TOFA (5-tetradecyl-oxy-2-furoic acid) decreases fat...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818041</comments>
            <pubDate>Fri, 13 May 2011 17:01:15 +0100</pubDate>
            <guid isPermaLink="false">4818041</guid>        </item>
        <item>
            <title>Evaluation of academic scientists' responses to situations that pose a conflict of interest.</title>
            <link>http://www.medworm.com/index.php?rid=4818040&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21525792%26dopt%3DAbstract</link>
            <description>Authors: Sax JK, Doran N
    The industry-academy relationship has many benefits, but it also has potential drawbacks, including potential conflicts of interest (e.g., when the profit motives of a private company unduly influence academic responsibilities). To date, policies intended to regulate or manage financial conflicts of interest appear to be unsatisfying and inadequate. The present study examined predictors of the responses of academic scientists and clinicians to hypothetical situations in which financial and other conflicts of interest may arise. Academic scientists and clinicians at five medical schools completed an anonymous survey that included vignettes that posed a potential conflict of interest. Participants indicated the likelihood that they would engage in specific action...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818040</comments>
            <pubDate>Fri, 13 May 2011 17:01:03 +0100</pubDate>
            <guid isPermaLink="false">4818040</guid>        </item>
        <item>
            <title>SOM230 combined with celecoxib prolongs the survival in nude mice with HepG-2 xenografts.</title>
            <link>http://www.medworm.com/index.php?rid=4818039&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21532334%26dopt%3DAbstract</link>
            <description>Authors: Xie Y, Chen S, Wang CH, Tang CW
    A new non-cytotoxic therapy that SOM230 (pasireotide)，a somatostatin analogue (SSTA) combined with celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor was tested in nude mice bearing HepG2 xenografts. Two agents did not markedly arrest the growth of HepG2 cells but greatly down-regulated vascular endothelial growth factor expression. An imbalance between the vigorous demand and insufficient supply of nutrients and oxygen for tumor growth resulted in the massive necrosis of xenografts. The combination synergistically induced the early apoptosis of HepG2 cells and achieved longest survival without adverse reaction. This impressive strategy appears promising as a systemic therapy for patients with hepatocellular carcinoma (HCC).
    PMID: 2...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818039</comments>
            <pubDate>Fri, 13 May 2011 17:00:53 +0100</pubDate>
            <guid isPermaLink="false">4818039</guid>        </item>
        <item>
            <title>L-carnitine ameliorates cancer cachexia in mice by regulating the expression and activity of carnitine palmityl transferase.</title>
            <link>http://www.medworm.com/index.php?rid=4818038&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21532335%26dopt%3DAbstract</link>
            <description>Authors: Liu S, Wu HJ, Zhang ZQ, Chen Q, Liu B, Wu JP, Zhu L
    Cancer cachexia is characterized by progressive weight loss with the depletion of adipose tissue and skeletal muscle. Impaired fatty acid oxidation mainly resulting from the decrease of carnitine palmitoyltransferase I and II activities in the liver is an important factor that contributes to cancer cachexia . Although recent studies suggest a potential application of L-carnitine in treatment of cancer cachexia, the underlying mechanisms are unknown. In the present study, we aim to assess the effects of L-carnitine on the activity and expression of CPT I and II in the liver of cachectic cancer mice. Our results show that the inoculation of colon-26 adenocarcinoma cells into mice led to cancer cachexia characterized by notable ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818038</comments>
            <pubDate>Fri, 13 May 2011 17:00:45 +0100</pubDate>
            <guid isPermaLink="false">4818038</guid>        </item>
        <item>
            <title>Combination therapy of recurrent prostate cancer with the proteasome inhibitor Bortezomib plus hormone blockade.</title>
            <link>http://www.medworm.com/index.php?rid=4818037&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21532336%26dopt%3DAbstract</link>
            <description>Authors: Kraft AS, Garrett-Mayer E, Wahlquist AE, Golshayan A, Chen CS, Butler W, Bearden J, Lilly M
    A single arm phase II trial of single-agent bortezomib (BZM) alone or combined with hormone blockade was conducted in patients with early PSA recurrence after definitive local therapy. The primary endpoint of this study was to determine the time to PSA relapse after BZM therapy alone or when BZM was combined with hormone blockade. The secondary endpoint was to determine the safety of combination therapy. Part A of the treatment schedule consisted of three cycles of BZM 1.3 mg/m2 IV given on days 1,4,8,11. If patients progressed on Part A, they were entered on Part B which consisted of a single dose of LH-RH antagonist, daily oral antiandrogen, and weekly BZM 1.3 mg/m2 for three out of f...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818037</comments>
            <pubDate>Fri, 13 May 2011 17:00:39 +0100</pubDate>
            <guid isPermaLink="false">4818037</guid>        </item>
        <item>
            <title>Identification of STAT3-independent regulatory effects for protein inhibitor of activated STAT3 by binding to novel transcription factors.</title>
            <link>http://www.medworm.com/index.php?rid=4818036&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21532337%26dopt%3DAbstract</link>
            <description>Authors: Dabir S, Kluge A, Dowlati A
    Protein Inhibitor of Activated Signal Transducer and Activators of Transcription 3 (PIAS3) is a molecule that regulates STAT3 and has antiproliferative properties. Glioblastoma and squamous cell lung cancer lack PIAS3 expression. To test the hypothesis that PIAS3 transcriptional effects are STAT3-independent, we developed models for STAT3 knockdown and PIAS3 over-expression. PIAS3 expression results in a distinct transcriptional profile that does not occur with STAT3 knockdown. We identify novel transcription factor binding partners for PIAS3 including ETS, EGR1, NR1I2, and GATA1. PIAS3 binds to these factors and regulates their transcriptional effects resulting in alterations in canonical pathways including Wnt/β-catenin signaling and functions su...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818036</comments>
            <pubDate>Fri, 13 May 2011 17:00:34 +0100</pubDate>
            <guid isPermaLink="false">4818036</guid>        </item>
        <item>
            <title>Oral RKS262 reduces tumor burden in a neuroblastoma xenograft animal model and mediates cytotoxicity through SAPK/JNK and ROS activation in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=4818035&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21532338%26dopt%3DAbstract</link>
            <description>Authors: Singh RK, Dorf L, Demartino A, Illenye S, Koto K, Currier EA, Ashikaga T, Kim KK, Brard L, Saulnier Sholler GL
    Patients diagnosed with high-risk neuroblastoma (NB), an extracranial solid tumor in children, have metastases and low survival (30%) despite aggressive multi-modal therapy. Therefore new therapies are urgently needed. We show significant in vitro and in vivo antitumor efficacy of RKS262 in NB. RKS262 showed superior cytotoxicity (IC50 = 6-25μM) against six representative NB cell lines compared to its parent analog Nifurtimox (currently in phase 2). Pre-formulated RKS262 (150mg/kg/daily) pellets administered orally, suppressed tumor growth (60%, p = 0.021) in NB xenograft mice within 28 days. RKS262-treated SMSKCNR cells showed TUNEL-positive DNA nicks and activation...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818035</comments>
            <pubDate>Fri, 13 May 2011 17:00:30 +0100</pubDate>
            <guid isPermaLink="false">4818035</guid>        </item>
        <item>
            <title>Gallotannin inhibits NF-ĸB signaling and growth of human colon cancer xenografts.</title>
            <link>http://www.medworm.com/index.php?rid=4818034&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21532339%26dopt%3DAbstract</link>
            <description>Authors: Al-Halabi R, Bou Chedid M, Abou Merhi R, El-Hajj H, Zahr H, Schneider-Stock R, Bazarbachi A, Gali-Muhtasib H
    Gallotannin (GT), the polyphenolic hydrolyzable tannin, exhibits anti-inflammatory and anticancer activities through mechanisms that are not fully understood. Several effects modulated by GT have been shown to be linked to interference with inflammatory mediators. Considering the central role of nuclear factor kappa B (NF-ĸB) in inflammation and cancer, we investigated the effect of GT on NF-ĸB signaling in HT-29 and HCT-116 human colon cancer cells. DNA binding assays revealed significant suppression of tumor necrosis factor (TNF-α)-induced NF-ĸB activation which correlated with the inhibition of IĸBα phosphorylation and degradation. Sequentially, p65 nuclear tra...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818034</comments>
            <pubDate>Fri, 13 May 2011 17:00:25 +0100</pubDate>
            <guid isPermaLink="false">4818034</guid>        </item>
        <item>
            <title>RON (MST1R) is a novel prognostic marker and therapeutic target for gastroesophageal adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4818033&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21543897%26dopt%3DAbstract</link>
            <description>Authors: Catenacci DV, Cervantes G, Yala S, Nelson EA, El-Hashani E, Kanteti R, El Dinali M, Hasina R, Brägelmann J, Seiwert T, Sanicola M, Henderson L, Grushko TA, Olopade O, Karrison T, Bang YJ, Kim WH, Tretiakova M, Vokes E, Frank DA, Kinder HL, Huet H, Salgia R
    RON (MST1R) is one of two members of the MET receptor tyrosine kinase family, along with parent receptor MET. RON has a putative role in several cancers, but its expression and function is poorly characterized in gastroesophageal adenocarcinoma. A recognized functional role of MET tyrosine kinase in gastroesophageal cancer has led to early phase clinical trials using MET inhibitors, with unimpressive results. Therefore, the role of RON in gastroesophageal cancer, as well as its role in cooperative signaling with MET and as ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818033</comments>
            <pubDate>Fri, 13 May 2011 17:00:19 +0100</pubDate>
            <guid isPermaLink="false">4818033</guid>        </item>
        <item>
            <title>Breast cancer stem-like cells show dominant homologous recombination due to a larger S- G2 fraction.</title>
            <link>http://www.medworm.com/index.php?rid=4818032&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21558789%26dopt%3DAbstract</link>
            <description>In this study, we examined a possible mechanism that might underlie this phenotype by looking at cell cycle profile and the effect this has on DNA repair pathways. The cell cycle profile showed that there were more CD24 (-) ESA (+) sorted MDA-MB231 cells in the S- and G2-phases compared with the unsorted cells, 60 and 38% respectively. Cyclin D and E protein levels supported the cell cycle profile and highlighted the possible involvement of homologous recombination (HR) repair in the radioresistant phenotype. To further support this, CD24- ESA+ sorted MDA-MB231 cells demonstrated statistically significant more RAD51 and less γ-H2AX foci 2 h post 4Gy ionising radiation, compared with the unsorted population. Inhibition of the HR pathway effectively sterilised the CD24 (- ) ESA (+) sorted M...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4818032</comments>
            <pubDate>Fri, 13 May 2011 17:00:10 +0100</pubDate>
            <guid isPermaLink="false">4818032</guid>        </item>
        <item>
            <title>Inactivation of Brca2 cooperates with Trp53R172H to induce invasive pancreatic ductal adenocarcinomas in mice: A mouse model of familial pancreatic cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4711304&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21455033%26dopt%3DAbstract</link>
            <description>Authors: Feldmann G, Collins K, Dal Molin M, Duringer S, Volkmann P, Bartsch DK, Bisht S, Koorstra JB, Brossart P, Maitra A, Fendrich V
    Abstract An inactivating germline mutation in BRCA2 is the most common known genetic basis for familial pancreatic cancer (FPC), accounting for 5-10% of inherited cases. A genetically engineered mouse model of pancreatic ductal adenocarcinoma (PDAC) arising on the backdrop of Brca2 deficiency is likely to elucidate valuable diagnostic and therapeutic insights for FPC. Both Brca2 alleles were conditionally deleted during development within the pancreatic epithelium by generating Pdx1-Cre; Brca2f/f (&quot;CB&quot;) mice; in addition, triple transgenic Pdx1-Cre; Brca2f/f; LSL-Trp53R172H (&quot;CBP&quot;) mice were generated, in order to determine the impact of p53 deregulati...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711304</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:59 +0100</pubDate>
            <guid isPermaLink="false">4711304</guid>        </item>
        <item>
            <title>Studies on the inhibition of feline EGFR in squamous cell carcinoma: Enhancement of radiosensitivity and rescue of resistance to small molecule inhibitors.</title>
            <link>http://www.medworm.com/index.php?rid=4711303&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21464610%26dopt%3DAbstract</link>
            <description>This study investigated different methods of EGFR (Epithelial Growth Factor Receptor) targeting in feline squamous cell carcinoma with the ultimate aim of establishing a large animal model of human head and neck cancer. Both small molecule receptor tyrosine kinase inhibitor (TKI) and RNA interference (RNAi) techniques were employed to target the feline EGFR. We demonstrated that the human drug gefitinib caused a reduction in cell proliferation and migration in a feline cell line. However, we also document the development of resistance that was not associated with mutation in the kinase domain. RNAi caused a potent reduction in EGFR activity and was able to overcome acquired gefitinib resistance. In addition, RNAi targeting of EGFR, but not gefitinib, caused an additive effect on cell killi...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711303</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:54 +0100</pubDate>
            <guid isPermaLink="false">4711303</guid>        </item>
        <item>
            <title>Doxorubicin and daunorubicin induce processing and release of interleukin-1β through activation of the NLRP3 inflammasome.</title>
            <link>http://www.medworm.com/index.php?rid=4711302&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21464611%26dopt%3DAbstract</link>
            <description>Authors: Sauter KA, Wood LJ, Wong J, Iordanov M, Magun BE
    Anthracyclines including doxorubicin and daunorubicin are commonly used for the treatment of both hematologic and solid tumors. Dose related adverse effects often limit the effectiveness of anthracyclines in chemotherapy. Drug-related systemic inflammation mediated by interleukin-1 beta (IL-1β) has been implicated in contributing to these adverse effects. The molecular mechanisms underlying anthracycline-mediated expression and IL-1β release are not understood. Elucidating the molecular basis by which anthracyclines upregulate IL-1β activity may present opportunities to decrease the inflammatory consequences of these drugs. Here we demonstrate that doxorubicin induces a systemic increase in IL-1β and other inflammatory cytok...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711302</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:47 +0100</pubDate>
            <guid isPermaLink="false">4711302</guid>        </item>
        <item>
            <title>Monoclonal antibodies for copper-64 PET dosimetry and radioimmunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=4711301&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21464612%26dopt%3DAbstract</link>
            <description>Conclusions: PET imaging allows the use of ( 64) Cu for pre-therapy calculation of tumor dosimetry. In spite of highly similar tumor dosimetry, an internalizing antibody did not improve the outcome of ( 64) Cu radioimmunotherapy. Radioresistance of this tumor cell line and copper efflux may have confounded the study. Further investigations of the 2 therapeutic efficacy of ( 64) Cu-labeled mAbs will focus on interaction between 64Cu and tumor suppressor genes and copper chaperones.
    PMID: 21464612 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711301</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:42 +0100</pubDate>
            <guid isPermaLink="false">4711301</guid>        </item>
        <item>
            <title>Comparison of the effects of the PI3K/mTOR inhibitors NVP-BEZ235 and GSK2126458 on tamoxifen-resistant breast cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4711300&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21464613%26dopt%3DAbstract</link>
            <description>Conclusion: Increased resistance to tamoxifen in these MCF-7 sub-lines is not associated with hypersensitivity to PI3K inhibitors. While both drugs inhibited AKT signaling, NVP-BEZ235 resembled rapamycin in inhibiting the mTOR pathway.
    PMID: 21464613 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711300</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:37 +0100</pubDate>
            <guid isPermaLink="false">4711300</guid>        </item>
        <item>
            <title>The PTEN/PI3K/Akt pathway regulates stem-like cells in primary esophageal carcinoma cells.</title>
            <link>http://www.medworm.com/index.php?rid=4711299&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21467840%26dopt%3DAbstract</link>
            <description>This study indicates that SP cells in primary culture cells from tissue specimens could be a promising model for cancer stem cell research and may help researchers develop novel therapeutic strategies or efficient drugs that target ESCC stem-like cells.
    PMID: 21467840 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711299</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:32 +0100</pubDate>
            <guid isPermaLink="false">4711299</guid>        </item>
        <item>
            <title>Regulatory dendritic cells: New targets for cancer immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=4711298&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21474998%26dopt%3DAbstract</link>
            <description>Authors: Shurin MR, Naiditch H, Zhong H, Shurin GV
    Commentary to:: A new tumor vaccine: FAPτ-MT elicits effective antitumor response by targeting Indolamine2, 3-dioxygenase in antigen presenting cells : Yan-Mei Yi, Ge Zhang, Jun Zeng, Si-Chao Huang, Ling-Ling Li, Rui Fang,Guan-Min Jiang, Xian-Zhang Bu, Shao-Hui Cai and Jun Du.
    PMID: 21474998 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711298</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:25 +0100</pubDate>
            <guid isPermaLink="false">4711298</guid>        </item>
        <item>
            <title>Advances in understanding regulatory myeloid cells.</title>
            <link>http://www.medworm.com/index.php?rid=4711297&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21474999%26dopt%3DAbstract</link>
            <description>Authors: Romano A, Vetro C, Adriani M
    The Regulatory Myeloid Cells - International Immunopharmacology Conference in October 21-24, 2010 reviewed the recent advances in our understanding of the biological mechanisms of expansion, activation, metabolism and mechanisms of T-cell suppression of Myeloid Derived Suppressor Cells (MDSC). Lectures were focused on the control of the microenvironment and cytokines needed for myelopoiesis, interactions with the neoplastic surrounding cells for a negative immune control, and the role of MDSC in cancer promotion. The complexity of the tumor microenvironment and opportunities for therapeutic interventions by targeting, and/or manipulating MDSCs was emphasized. A better understanding of the crosstalk between myelo- and lymphoid arms of the immune sys...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711297</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:18 +0100</pubDate>
            <guid isPermaLink="false">4711297</guid>        </item>
        <item>
            <title>Diagnostic values of SCC, CEA, Cyfra21-1 and NSE for lung cancer in patients with suspicious pulmonary masses: A single center analysis.</title>
            <link>http://www.medworm.com/index.php?rid=4711296&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21483235%26dopt%3DAbstract</link>
            <description>Authors: Chu XY, Hou XB, Song WA, Xue ZQ, Wang B, Zhang LB
    We recruited 805 patients with suspicious pulmonary masses that were identified finally as lung cancer or benign pulmonary masses. The serum levels of four tumor markers, including squamous cell carcinoma antigen (SCC), carcinoembryonic antigen (CEA), cytokeratin 19 fragment antigen 21-1 (Cyfra21-1) and neuron specific enolase (NSE) were tested for every patient. Though receiver operating characteristic (ROC) curves indicated unsatisfactory diagnostic power of those four tumor markers for lung cancer, 37.3% of early-staged lung cancer could be diagnosed just on the combination assays of the four tumor markers, under adjusted cut-off values through our statistical analysis retrospectively.
    PMID: 21483235 [PubMed - as supplie...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4711296</comments>
            <pubDate>Thu, 14 Apr 2011 22:00:10 +0100</pubDate>
            <guid isPermaLink="false">4711296</guid>        </item>
        <item>
            <title>Validating the use of a luciferase labeled breast cancer cell line, MDA435LCC6, as a means to monitor tumor progression and to assess the therapeutic activity of an established anticancer drug, docetaxel (Dt) alone or in combination with the ILK inhibitor, QLT0267.</title>
            <link>http://www.medworm.com/index.php?rid=4593728&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21358264%26dopt%3DAbstract</link>
            <description>Authors: Kalra J, Anantha M, Warburton C, Waterhouse D, Yang H, Yang YJ, Strut D, Osooly M, Masin D, Bally MB
    A significant issue in drug efficacy studies is animal study design. Here we hypothesize that when evaluating new or existing therapeutics for the treatment of cancer, the location of disease burden will influence drug efficacy. To study this, Female NCr nude mice were inoculated with luciferase-positive human breast cancer cells (LCC6WT-luc) orthotopically (o.t.), intraperitoneally (i.p.) or intracardiacly (i.c.) to create localized, ascites or disseminated disease, respectively. Tumor development was monitored using bioluminescence imaging. Docetaxel (Dt) pharmacokinetics and distribution to sites of tumor growth were determined. Disease progression was followed in animals tr...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593728</comments>
            <pubDate>Wed, 16 Mar 2011 15:16:26 +0100</pubDate>
            <guid isPermaLink="false">4593728</guid>        </item>
        <item>
            <title>Mesenchymal stem cells expressing GD2 and CD271 correlate with breast cancer-initiating cells in bone marrow.</title>
            <link>http://www.medworm.com/index.php?rid=4593727&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21358274%26dopt%3DAbstract</link>
            <description>Conclusions: There was a positive correlation between mesenchymal stem cells expressing GD2 and CD271 and breast cancer-initiating cells in BM of patients with primary breast cancer.
    PMID: 21358274 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593727</comments>
            <pubDate>Wed, 16 Mar 2011 15:16:22 +0100</pubDate>
            <guid isPermaLink="false">4593727</guid>        </item>
        <item>
            <title>Chitosan hydrogel for localized gene silencing.</title>
            <link>http://www.medworm.com/index.php?rid=4593726&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21358280%26dopt%3DAbstract</link>
            <description>Conclusions: This study developed a novel local delivery method for siRNA therapy using the CH-HG system. This approach could have broad applications for multiple localized diseases.
    PMID: 21358280 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593726</comments>
            <pubDate>Wed, 16 Mar 2011 15:16:17 +0100</pubDate>
            <guid isPermaLink="false">4593726</guid>        </item>
        <item>
            <title>Estrogen-induced dimerization and activation of ERα-fused caspase-8: Artificial reversal of the estrogenic hormone effect in carcinogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=4593725&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21364316%26dopt%3DAbstract</link>
            <description>Authors: Zhao ZN, Zhou Q, Bai JX, Yan B, Qin WW, Wang T, Li Y, Yang AG, Jia LT
    The cascade of caspase processing and activation is the core of apoptotic cell signaling. Initiator caspases are activated by adaptor-mediated clustering, which allows the intermolecular autoprocessing of the zymogens in close proximity. Caspase-8, the prototypical initiator critically involved in apoptosis induced by varied extrinsic stimuli, is physiologically recruited via a classical FasL/Fas/FADD pathway. Meanwhile, artificial models of caspase-8 activation have been proposed via inducible dimerization of a heterologous domain fused to the zymogen. Here, we describe the generation of a chimeric protein of caspase-8 and the ligand-binding domain (LBD) of estrogen receptor α (ERα), which dimerizes and u...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593725</comments>
            <pubDate>Wed, 16 Mar 2011 15:16:13 +0100</pubDate>
            <guid isPermaLink="false">4593725</guid>        </item>
        <item>
            <title>Role of GPR30 in testicular germ cell tumors: A potential new anticancer target.</title>
            <link>http://www.medworm.com/index.php?rid=4593724&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21372633%26dopt%3DAbstract</link>
            <description>Authors: Vitale G, Dicitore A, Sciortino G, Abbruzzese A, Persani L, Santini D
    Commentary to: : GPR30 is overexpressed in post puberal testicular germ cell tumors : Renato Franco, Francesca Boscia, Vincenzo Gigantino, Laura Marra, Francesco Esposito, Diana Ferrara, Paolo Pariante, Gerardo Botti, Michele Caraglia, Sergio Minucci and Paolo Chieffi.
    PMID: 21372633 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593724</comments>
            <pubDate>Wed, 16 Mar 2011 15:16:06 +0100</pubDate>
            <guid isPermaLink="false">4593724</guid>        </item>
        <item>
            <title>Solid phase synthesis, radiolabeling and biological evaluation of a ( 99m) Tc-labeled αVβ3 tripeptide (RGD) conjugated to DOTA as a tumor imaging agent.</title>
            <link>http://www.medworm.com/index.php?rid=4593722&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21372636%26dopt%3DAbstract</link>
            <description>Authors: Varshney R, Hazari PP, Uppal JK, Pal S, Stromberg R, Allard M, Mishra AK
    Solid phase synthesis of peptides-radiometal chelator can facilitate the creation of radioactive peptide libraries to be utilized in high throughput in in vivo screening of targeted molecular imaging agents. An αVβ3 tripeptide derivative DOTA-NH-Arg-Gly-Asp was synthesized by Fmoc solid phase peptide synthesis and analyzed by spectroscopic techniques. In order to radiolabel this RGD peptide with 99mTc-1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA) was incorporated as a chelator. The DOTA-peptide conjugate binds to 99mTc with high efficiency at ambient temperature. The resulting conjugate is stable under physiological conditions for at least 24 h after radiocomplexation. The receptor bin...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593722</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:53 +0100</pubDate>
            <guid isPermaLink="false">4593722</guid>        </item>
        <item>
            <title>A new tumor vaccine: FAPτ-MT elicits effective antitumor response by targeting Indolamine2, 3-dioxygenase in antigen presenting cells.</title>
            <link>http://www.medworm.com/index.php?rid=4593719&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21372637%26dopt%3DAbstract</link>
            <description>In this study, we developed a new tumor vaccine, FAPτ-MT, which was produced by conjugating 1-MT to a tumor associated antigen, fibroblast activation protein α (FAPα). The results in vitro confirmed that 1-MT could be dissociated from the FAPτ-MT vaccine and inhibit intracellular IDO activity. In an FAPα-positive tumor model, the FAPτ-MT vaccine elicited an anti-tumor response which was similar to systemic treatment with the FAPτ vaccine plus 1-MT. Most importantly, administration of the FAPτ-MT vaccine did not lead to pregnancy failiure in mice carrying allogeneic fetuses. These findings that FAPτ-MT breaks tumor immune tolerance as a local IDO inhibitor, suggest that conjugation of 1-MT to a tumor antigen peptide is a potentially effective clinical cancer immunotherapy.
    PMID...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593719</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:45 +0100</pubDate>
            <guid isPermaLink="false">4593719</guid>        </item>
        <item>
            <title>Methylated genes in breast cancer: Associations with clinical and histopathological features in a familial breast cancer cohort.</title>
            <link>http://www.medworm.com/index.php?rid=4593714&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21383541%26dopt%3DAbstract</link>
            <description>Conclusion: We report several novel, positive associations between percent methylation of the APC, RASSF1A, TWIST, ERα, CDH1, and Cyclin D2 genes and key variables such as tumor stage, hormone and growth receptor status, and a history of recurrent or metastatic disease. Our data suggest the potential utility of parsing gene methylation by functional status and breast tumor subtype.
    PMID: 21383541 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593714</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:40 +0100</pubDate>
            <guid isPermaLink="false">4593714</guid>        </item>
        <item>
            <title>Synergistic therapeutic effect in gastric cancer cells produced by oncolytic adenovirus encoding Drosophila melanogaster deoxyribonucleoside kinase.</title>
            <link>http://www.medworm.com/index.php?rid=4593711&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21383545%26dopt%3DAbstract</link>
            <description>Authors: Zhu Z, Mao L, Zhao L, Sun Z, Wang Z, Xu H, Zheng X
    Drosophila melanogaster multisubstrate deoxyribonucleoside kinase (Dm-dNK), a novel suicide kinase, was applied as a cancer gene therapeutic approach. To improve the antitumor effect of Dm-dNK and its substrate with the selectivity and safety control in consideration, the conditionally replicative gene-viral system ZD55-dNK, which includes the replicationselective adenovirus ZD55 armed with the Dm-dNK, was used to further explore the potential of this approach. When ZD55-dNK was combined with BVDU it produced a synergistic inhibitive effect of adenovirus replication in vitro while maintaining specific cancer cell killing activity. From a clinical standpoint, this approach is promising for its considerably low toxic side effect...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593711</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:34 +0100</pubDate>
            <guid isPermaLink="false">4593711</guid>        </item>
        <item>
            <title>The analysis of organic anion transporting polypeptide (OATP) mRNA and protein patterns in primary and metastatic liver cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4593710&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21383546%26dopt%3DAbstract</link>
            <description>Authors: Wlcek K, Svoboda M, Riha J, Zakaria S, Olszewski U, Dvorak Z, Sellner F, Ellinger I, Jäger W, Thalhammer T
    Organic anion transporting polypeptides (OATP, SLCO genes) mediate the uptake of endobiotics and drugs. Thus, their expression levels and pattern could be of relevance for cancer therapy. This prompted us to investigate the expression of poorly characterized OATPs, namely OATP2A1, OATP3A1, OATP4A1 and OATP5A1 in hepatic cancer of different origin. First, mRNA levels of all eleven OATPs were determined in paired (cancerous and adjacent non-cancerous) specimens from 43 patients with primary liver cancer (hepatocellular carcinoma, HCC; cholangiocellular carcinoma, CCC) and liver metastases from colon tumors (MLT). Real-time RT-PCR analysis revealed that all OATPs, except OA...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593710</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:29 +0100</pubDate>
            <guid isPermaLink="false">4593710</guid>        </item>
        <item>
            <title>The antiandrogenic effect of finasteride against a mutant androgen receptor.</title>
            <link>http://www.medworm.com/index.php?rid=4593709&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21386657%26dopt%3DAbstract</link>
            <description>Authors: Wu Y, Chhipa RR, Zhang H, Ip C
    Finasteride is known to inhibit Type 2 5α-reductase and thus block the conversion of testosterone to dihydrotestosterone (DHT). The structural similarity of finasteride to DHT raises the possibility that finasteride may also interfere with the function of the androgen receptor (AR). Experiments were carried out to evaluate the antiandrogenic effect of finasteride in LNCaP, C4-2 and VCaP human prostate cancer cells. Finasteride decreased DHT binding to AR, and DHT-stimulated AR activity and cell growth in LNCaP and C4-2 cells, but not in VCaP cells. LNCaP and C4-2 (derived from castration-resistant LNCaP) cells express the T877A mutant AR, while VCaP cells express the wild type AR. When PC-3 cells, which are AR-null, were transfected with either ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593709</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:25 +0100</pubDate>
            <guid isPermaLink="false">4593709</guid>        </item>
        <item>
            <title>A magnifying glass on glioblastoma stem cell signaling pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4593708&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21386658%26dopt%3DAbstract</link>
            <description>Authors: Bell D, Miele L
    Commentary to:: β-catenin and Gli1 are prognostic markers in glioblastoma : Marco Rossi, Letizia Magnoni, Clelia Miracco, Elisa Mori, Piero Tosi, Luigi Pirtoli, Paolo Tini, Giuseppe Oliveri, Elena Cosci and Annette Bakker.
    PMID: 21386658 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593708</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:21 +0100</pubDate>
            <guid isPermaLink="false">4593708</guid>        </item>
        <item>
            <title>EMT: A new vision of hypoxia promoting cancer progression.</title>
            <link>http://www.medworm.com/index.php?rid=4593707&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21389772%26dopt%3DAbstract</link>
            <description>Authors: Jiang J, Tang YL, Liang XH
    A hypoxic microenvironment plays a critical role in the development and progression of tumors. The epithelial to mesenchymal transition (EMT) is a process by which epithelial cells lose their polarity and are converted to a mesenchymal phenotype, which is regarded as a critical event in morphogenetic changes during embryonic development, wound healing, and cancer metastasis. Recent advances in our understanding of the molecular pathways that govern the association of hypoxia with malignant tumors point to the epithelial to mesenchymal transition (EMT). The hypoxic microenvironment common to cancer cells emerges as an important factor in the induction of a pathological EMT, which is a key link in cancer progression. This review presents the potential ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593707</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:17 +0100</pubDate>
            <guid isPermaLink="false">4593707</guid>        </item>
        <item>
            <title>Potent genistein derivatives as inhibitors of estrogen receptor alpha-positive breast cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4593706&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21389782%26dopt%3DAbstract</link>
            <description>Authors: Marik R, Allu M, Anchoori R, Stearns V, Umbricht CB, Khan S
    The estrogen receptor (ER) is a major target for the treatment of breast cancer cells. Genistein, a soy isoflavone, possesses a structure similar to estrogen and can both mimic and antagonize estrogen effects although at high concentrations it inhibits breast cancer cell proliferation. Hence, to enhance the anti-cancer activity of Genistein at lower concentrations, we have synthesized seven structurally modified derivatives of Genistein (MA-6, MA-8, MA-11, MA-19, MA-20, MA-21 and MA-22) based on the structural requirements for an optimal anti-cancer effect. Among those seven, three derivatives (MA-6, MA-8 and MA-19) showed high antiproliferative activity with IC 50 levels in the range of 1-2.5 μM, i.e., at much lower...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4593706</comments>
            <pubDate>Wed, 16 Mar 2011 15:15:12 +0100</pubDate>
            <guid isPermaLink="false">4593706</guid>        </item>
        <item>
            <title>Expression and localization of the uptake transporters OATP2B1, OATP3A1 and OATP5A1 in non-malignant and malignant breast tissue.</title>
            <link>http://www.medworm.com/index.php?rid=4481972&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278488%26dopt%3DAbstract</link>
            <description>Authors: Kindla J, Rau TT, Jung R, Fasching PA, Strick R, Stoehr R, Hartmann A, Fromm MF, König J
    Organic anion transporting polypeptides (OATPs, gene family SLCO/SLC21) mediate the uptake of multiple endogenous substances such as estrogens and estrogen metabolites and of several widely prescribed drugs (e.g. statins, antibiotics and anticancer agents) into cells. Since several anticancer agents have been identified as substrates for OATPs, these transporters may also have an impact on cancer treatment. Expression of OATPs has been identified in colon, pancreatic and gastric carcinomas but to date little is known about the expression and localization of OATP family members in non-malignant breast tissue and breast cancer. We therefore analyzed the mRNA expression of all human OATP fam...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481972</comments>
            <pubDate>Wed, 16 Feb 2011 06:47:41 +0100</pubDate>
            <guid isPermaLink="false">4481972</guid>        </item>
        <item>
            <title>GPR30 is over-expressed in post puberal testicular germ cell tumors.</title>
            <link>http://www.medworm.com/index.php?rid=4481971&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278491%26dopt%3DAbstract</link>
            <description>In this study, we have evaluated by immunohistochemical analysis GPR30 expression in post-puberal testicular germ cell tumours (30 seminomas, 5 teratomas, 12 embryonal carcinomas, and 20 intratubular germ cell tumors). The GPR30 protein expression was detected at high level in all intratubular germ cell tumours, seminomas, and embryonal carcinomas, whereas in teratomas the expression was low. The immunohistochemical data were further confirmed by Western blot analysis. GPR30 protein expression has also been analyzed in GC1 and TCam-2 cell lines, respectively derived from immortalized type B murine spermatogonia and human seminoma. Our results indicate that GPR30 could be a potential therapeutic target; the design of a specific GPR30 inhibitors could be a useful molecular target to block ne...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481971</comments>
            <pubDate>Wed, 16 Feb 2011 06:47:37 +0100</pubDate>
            <guid isPermaLink="false">4481971</guid>        </item>
        <item>
            <title>c-Myc induction of programmed cell death may contribute to carcinogenesis: A perspective inspired by several concepts of chemical carcinogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=4481970&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21278493%26dopt%3DAbstract</link>
            <description>Authors: Wang C, Tai Y, Lisanti MP, Liao DJ
    The c-Myc protein, encoded by c-myc gene, in its wild-type form can induce tumors with a high frequency and can induce massive programmed cell death (PCD) in most transgenic mouse models, with greater efficiency than other oncogenes. Evidence also indicates that c-Myc can cause proliferative inhibition, i.e. mitoinhibition. The c-Myc-induced PCD and mitoinhibition, which may be attributable to its inhibition of cyclin D1 and induction of p53, may impose a pressure of compensatory proliferation, i.e. regeneration, onto the initiated cells (cancer progenitor cells) that occur sporadically and are resistant to the mitoinhibition. The initiated cells can thus proliferate robustly and progress to a malignancy. This hypothetical thinking, i.e. the ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481970</comments>
            <pubDate>Wed, 16 Feb 2011 06:47:33 +0100</pubDate>
            <guid isPermaLink="false">4481970</guid>        </item>
        <item>
            <title>Knockdown of ezrin via RNA interference suppresses Helicobacter pylori-enhanced invasion of gastric cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4481969&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21282970%26dopt%3DAbstract</link>
            <description>Conclusion: Knockdown of ezrin by RNAi suppresses H. pylori-enhanced migration and invasion of gastric cancer cells. These findings indicate that ezrin may play a key role in the migration and invasion of gastric cancer cells, and thus may be a therapeutic target to prevent metastasis of gastric cancer promoted by H. pylori infection.
    PMID: 21282970 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481969</comments>
            <pubDate>Wed, 16 Feb 2011 06:47:27 +0100</pubDate>
            <guid isPermaLink="false">4481969</guid>        </item>
        <item>
            <title>Augmentation of tumor-specific immunity by upregulation of apoptotic melanoma cell calreticulin expression.</title>
            <link>http://www.medworm.com/index.php?rid=4481968&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21282973%26dopt%3DAbstract</link>
            <description>Authors: Mosca P, Robertson GP
    Commentary to: Melanoma B16-F1 cells coated with fusion protein of mouse calreticulin and virus G-protein coupled receptor induced the antitumor immune response in Balb/C mice Yi Qin, Yu Han, Chunyu Cao, Yushan Ren, Chunhong Li and Yanlin Wang.
    PMID: 21282973 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481968</comments>
            <pubDate>Wed, 16 Feb 2011 06:47:17 +0100</pubDate>
            <guid isPermaLink="false">4481968</guid>        </item>
        <item>
            <title>Bortezomib treatment causes remission in a Ph+ ALL patient and reveals FoxO as a theranostic marker.</title>
            <link>http://www.medworm.com/index.php?rid=4481967&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21282974%26dopt%3DAbstract</link>
            <description>This study provides support that FoxO3 is a good biomarker for BCR-ABL-mediated leukemogenesis. Additionally, proteasomal inhibition by bortezomib may be a promising therapeutic option in Philadelphia-positive ALL, where FoxO3 is downregulated.
    PMID: 21282974 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481967</comments>
            <pubDate>Wed, 16 Feb 2011 06:47:07 +0100</pubDate>
            <guid isPermaLink="false">4481967</guid>        </item>
        <item>
            <title>Molecular mechanisms of resistance to the EGFR monoclonal antibody cetuximab.</title>
            <link>http://www.medworm.com/index.php?rid=4481966&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21293176%26dopt%3DAbstract</link>
            <description>Authors: Brand TM, Iida M, Wheeler DL
    The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase belonging to the HER family of receptor tyrosine kinases. Receptor activation upon ligand binding leads to down stream activation of the PI3K/AKT, RAS/RAF/MEK/ERK and PLCγ/PKC pathways that influence cell proliferation, survival and the metastatic potential of tumor cells. Increased activation by gene amplification, protein overexpression or mutations of the EGFR has been identified as an etiological factor in a number of human epithelial cancers (e.g., NSCLC, CRC, glioblastoma and breast cancer). Therefore, targeting the EGFR has been intensely pursued as a cancer treatment strategy over the last two decades. To date, five EGFR inhibitors, including three small molecule tyr...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481966</comments>
            <pubDate>Wed, 16 Feb 2011 06:47:00 +0100</pubDate>
            <guid isPermaLink="false">4481966</guid>        </item>
        <item>
            <title>Histone deacetylase 1 is required for exocrine pancreatic epithelial proliferation in development and cancer.</title>
            <link>http://www.medworm.com/index.php?rid=4481965&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21301206%26dopt%3DAbstract</link>
            <description>This study indicates that HDAC1 is required for pancreatic epithelial proliferation in development and cancer. We hypothesize that aberrant expression of HDAC1 modulates the developmental and signaling pathways in exocrine pancreatic epithelia and consequently the genes required for cellular proliferation during development and progression of pancreatic neoplasia.
    PMID: 21301206 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481965</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:54 +0100</pubDate>
            <guid isPermaLink="false">4481965</guid>        </item>
        <item>
            <title>Targeting tumors that lack methylthioadenosine phosphorylase (MTAP) activity: Current strategies.</title>
            <link>http://www.medworm.com/index.php?rid=4481964&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21301207%26dopt%3DAbstract</link>
            <description>Authors: Bertino JR, Waud WR, Parker WB, Lubin M
    Many solid tumors and hematologic malignancies lack expression of the enzyme methylthioadenosine phosphorylase (MTAP), due either to deletion of the MTAP gene or to methylation of the MTAP promoter. In cells that have MTAP, its natural substrate, methylthioadenosine (MTA), generated during polyamine biosynthesis, is cleaved to adenine and 5-methylthioribose-1-phosphate. The latter compound is further metabolized to methionine. Adenine and methionine are further metabolized and hence salvaged. In MTAP-deficient cells, however, MTA is not cleaved and the salvage pathway for adenine and methionine is absent. As a result, MTAP-deficient cells are more sensitive than MTAP-positive cells to inhibitors of de novo purine synthesis and to methion...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481964</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:50 +0100</pubDate>
            <guid isPermaLink="false">4481964</guid>        </item>
        <item>
            <title>Don't jump to rash conclusions.</title>
            <link>http://www.medworm.com/index.php?rid=4481963&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21304273%26dopt%3DAbstract</link>
            <description>Authors: Bebb G, Boland W, Melosky B
    Commentary to: Bivalent binding by intermediate affinity of nimotuzumab: A contribution to explain antibody clinical profile Greta Garrido, Ilia A. Tikhomirov, Ailem Rabasa, Eric Yang, Elías Gracia, Normando Iznaga, Luis E. Fernández, Tania Crombet, Robert Kerbel and Rolando Pérez.
    PMID: 21304273 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481963</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:44 +0100</pubDate>
            <guid isPermaLink="false">4481963</guid>        </item>
        <item>
            <title>Formosanin C-inhibited pulmonary metastasis through repression of matrix metalloproteinases on mouse lung adenocarcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4481962&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21304274%26dopt%3DAbstract</link>
            <description>Authors: Man S, Gao W, Zhang Y, Liu Z, Yan L, Huang L, Liu C
    Formosanin C (FC) isolated from Rhizoma Paridis, showed pro-apoptosis and immunoregulation with antitumor activity in cultured cells and animal systems. However, there is no report about its anti-metastatic effect on cancer cells. This research used the wound healing and the migration assay to detect the anti-invasive effect of FC on LA795 cells. Through the gelatin zymography assay and immunofluorescence analysis, FC showed suppression of enzyme activity of MMP-2 and MMP-9, and protein expression of MMP-1, -2, -3, -9 and -14 excreted from LA795 cells. Finally, FC exhibited much more effective inhibition of tumor growth and pulmonary metastasis in T739 mice than cisplatin did. Overall, the strong inhibition of MMP expression ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481962</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:38 +0100</pubDate>
            <guid isPermaLink="false">4481962</guid>        </item>
        <item>
            <title>New prospects for hepatocellular carcinoma therapy: Microwave ablation working together with cellular immunotherapy.</title>
            <link>http://www.medworm.com/index.php?rid=4481961&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307638%26dopt%3DAbstract</link>
            <description>Authors: Pan Q, Li Q
    Commentary to: Phase Ⅰ clinical study of combination therapy with microwave ablation and cellular immunotherapy in hepatocellular carcinoma Pei Zhou, Ping Liang, Baowei Dong, Xiaoling Yu, Zhiyu Han and Yingxin Xu.
    PMID: 21307638 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481961</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:33 +0100</pubDate>
            <guid isPermaLink="false">4481961</guid>        </item>
        <item>
            <title>Targeting NF-ĸB mediated breast cancer chemoresistance through selective inhibition of sphingosine kinase-2.</title>
            <link>http://www.medworm.com/index.php?rid=4481960&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307639%26dopt%3DAbstract</link>
            <description>Authors: Antoon JW, White MD, Slaughter EM, Davis JL, Khalili HS, Elliott S, Smith CD, Burow ME, Beckman BS
    Resistance to chemotherapy remains a significant obstacle in the treatment of hormone- independent breast cancer. Recent evidence suggests that altered sphingolipid signaling through increased sphingosine kinase activity may be an important mediator of breast cancer drug resistance. Sphingosine kinase-1 (Sphk1) is a proposed key regulator of breast cancer tumorigenesis, proliferation and resistance. There is, however, conflicting data on the role of sphingosine kinase-2 (Sphk2) in cancer biology and resistance, with some suggesting that Sphk2 has an opposing role to that of Sphk1. Here, we studied the effects of the novel selective Sphk2 inhibitor, ABC294640 (3-(4-chlorophenyl)-a...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481960</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:25 +0100</pubDate>
            <guid isPermaLink="false">4481960</guid>        </item>
        <item>
            <title>Sphingosine kinase: A promising cancer therapeutic target.</title>
            <link>http://www.medworm.com/index.php?rid=4481959&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307640%26dopt%3DAbstract</link>
            <description>Authors: Antoon JW, Beckman BS
    Commentary to: Antitumor activity of Sphingosine Kinase 2 inhibitor ABC294640 and sorafenib in hepatocellular carcinoma xenografts Vladimir Beljanski, Clayton S. Lewis and Charles D. Smith.
    PMID: 21307640 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481959</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:18 +0100</pubDate>
            <guid isPermaLink="false">4481959</guid>        </item>
        <item>
            <title>A new perspective on Estrogen Receptor beta in breast cancer progression.</title>
            <link>http://www.medworm.com/index.php?rid=4481958&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307641%26dopt%3DAbstract</link>
            <description>Authors: Han L
    Commentary to: ERβ and PEA3 co-activate IL-8 expression and promote the invasion of breast cancer cells Ying Chen, Li Chen, Ji-Yu Li, Naofumi Mukaida, Qiaoqiao Wang, Chen Yang, Wen-Jin Yin, Xiao-Hua Zeng, Wei Jin and Zhi-ming Shao.
    PMID: 21307641 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481958</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:13 +0100</pubDate>
            <guid isPermaLink="false">4481958</guid>        </item>
        <item>
            <title>Probiotic factors partially improve parameters of 5-Fluorouracil-induced intestinal mucositis in rats.</title>
            <link>http://www.medworm.com/index.php?rid=4481957&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307648%26dopt%3DAbstract</link>
            <description>Authors: Prisciandaro LD, Geier MS, Butler RN, Cummins AG, Howarth GS
    Certain live bacteria have demonstrated preliminary indications of efficacy for the treatment of chemotherapy-induced intestinal mucositis. However, probiotic derived supernatants (SN) have yet to be investigated in the mucositis setting. We evaluated SN from Escherichia coli Nissle 1917 (EcN) and Lactobacillus fermentum BR11 (BR11) for their capacity to decrease 5-Fluorouracil (5-FU)-induced damage in vivo. Female Dark Agouti rats were gavaged with 1mL of either SN or vehicle daily (days 0-8) and intraperitoneally injected with 5-FU (150mg/kg) on day 5 to induce mucositis. On day 9, animals were culled and intestinal tissues collected. Significantly lower histological damage scores were apparent in the jejunum of 5-...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481957</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:09 +0100</pubDate>
            <guid isPermaLink="false">4481957</guid>        </item>
        <item>
            <title>Malignant characteristics of circulating tumor cells and corresponding primary tumor in a patient with esophageal squamous cell carcinoma before and after surgery.</title>
            <link>http://www.medworm.com/index.php?rid=4481956&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307656%26dopt%3DAbstract</link>
            <description>We report the malignant characteristics of circulating tumor cells (CTCs) and the corresponding molecular features of the primary tumor in a patient with esophageal squamous cell carcinoma (ESCC). A 70-year-old male patient was diagnosed with TNM stage T3N0M0 ESCC. Before surgery, seven intact CTCs and 12 CTCs with a fragmented membrane were detected in 7.5 mL of peripheral blood by immunofluorescence staining. One week after radical resection of the primary tumor, four CTCs were identified in 7.5ml peripheral blood. All CTCs were confirmed as having a malignant phenotype by chromosomal analysis and routine cell staining. Ninety percent of the CTCs were found to have polysomic chromosomes 8 and 20 by fluorescence in situ hybridization (FISH). Immunofluorescence analysis showed that all of ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481956</comments>
            <pubDate>Wed, 16 Feb 2011 06:46:04 +0100</pubDate>
            <guid isPermaLink="false">4481956</guid>        </item>
        <item>
            <title>Resistance to HER2-directed antibodies and tyrosine kinase inhibitors: Mechanisms and clinical implications.</title>
            <link>http://www.medworm.com/index.php?rid=4481955&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307659%26dopt%3DAbstract</link>
            <description>Authors: Garrett JT, Arteaga CL
    The antibody trastuzumab and the tyrosine kinase inhibitor lapatinib are approved by the FDA for the treatment of HER2-overexpressing breast cancer. These anti-HER2 drugs are changing the natural history of HER2-overexpressing breast cancer. However, therapeutic resistance to trastuzumab or lapatinib, as either single-agents or in combination with chemotherapy in the metastatic setting, typically occurs within months of starting therapy. Several mechanisms of trastuzumab-resistance have been reported that include signaling from other HER receptors, signaling from receptor tyrosine kinases (RTKs) outside of the HER (ErbB) family, increased phosphatidylinositol 3-kinase signaling, and the presence of truncated forms of HER2. Mechanisms of resistance to lap...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481955</comments>
            <pubDate>Wed, 16 Feb 2011 06:45:57 +0100</pubDate>
            <guid isPermaLink="false">4481955</guid>        </item>
        <item>
            <title>Wild-type and mutant p53 proteins interact with mitochondrial caspase-3.</title>
            <link>http://www.medworm.com/index.php?rid=4481954&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21307660%26dopt%3DAbstract</link>
            <description>In this study, we sought to determine the identity of other mitochondrial p53-interacting proteins. Using immunoprecipitation from purified mitochondria followed by mass spectrometry we identified caspase-3 as a mitochondrial p53-interacting protein. Interestingly, we find that tumor-derived mutant forms of p53 retain the ability to interact with mitochondrial caspase-3. Further, we find evidence that these mutant forms of p53 may interfere with the ability of procaspase-3 to become proteolytically activated by caspase-9. The combined data suggest that tumor-derived mutants of p53 may be selected for in tumor cells due to their ability to bind and inhibit the activation of caspase-3.
    PMID: 21307660 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481954</comments>
            <pubDate>Wed, 16 Feb 2011 06:45:51 +0100</pubDate>
            <guid isPermaLink="false">4481954</guid>        </item>
        <item>
            <title>Targeting the insulin-like growth factor network in cancer therapy.</title>
            <link>http://www.medworm.com/index.php?rid=4481953&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21311212%26dopt%3DAbstract</link>
            <description>Authors: Heidegger I, Pircher A, Klocker H, Massoner P
    During the last decades, changes in the insulin-like growth factor (IGF) signaling have been related to the pathogenesis of cancer. Therefore, IGFs became highly attractive therapeutic cancer targets. Several drugs including monoclonal antibodies (mAB), small molecule tyrosine kinase inhibitors (RTKIs), anti-sense oligonucleotids (ASOs) and IGF-binding proteins (IGFBPs) targeting the IGF axis were developed. With over 60 ongoing clinical trials, the IGF1 receptor (IGF1R) is currently one of the most studied molecular targets in the field of oncology. In this review, we provide an overview on the IGF axis, its signaling pathways and its significance in neoplasia. We critically review the preclinical and clinical studies investigatin...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481953</comments>
            <pubDate>Wed, 16 Feb 2011 06:45:37 +0100</pubDate>
            <guid isPermaLink="false">4481953</guid>        </item>
        <item>
            <title>Ovarian cancer stem cells and inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=4481952&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21317559%26dopt%3DAbstract</link>
            <description>Authors: Mor G, Yin G, Chefetz I, Yang Y, Alvero A
    Epithelial ovarian cancer (EOC) is the fourth leading cause of cancer-related deaths in women in the United States and the leading cause of gynecologic cancer deaths. The major limiting factor in the treatment of ovarian cancer is recurrence and chemoresistance. Individuals who succumb to advanced-stage ovarian cancer inevitably become refractory to chemotherapy, resulting in disease progression and death. The source of recurrence and lack of response to chemotherapy is unknown. The focus of this review is to evaluate the question of recurrence and chemoresistance based on the concept of the cancer stem cells and inflammation.
    PMID: 21317559 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4481952</comments>
            <pubDate>Wed, 16 Feb 2011 06:45:10 +0100</pubDate>
            <guid isPermaLink="false">4481952</guid>        </item>
        <item>
            <title>Bivalent binding by intermediate affinity of nimotuzumab: A contribution to explain antibody clinical profile.</title>
            <link>http://www.medworm.com/index.php?rid=4350706&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21150278%26dopt%3DAbstract</link>
            <description>This study suggests an explanation for nimotuzumab clinical profile, whereby anti-tumor activity is obtained in absence of severe toxicities due to its properties of bivalent binding to EGFR.
    PMID: 21150278 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350706</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:30 +0100</pubDate>
            <guid isPermaLink="false">4350706</guid>        </item>
        <item>
            <title>Intravenous liposomal delivery of the short hairpin RNAs against Plk1 controls the growth of established human hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4350705&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21150280%26dopt%3DAbstract</link>
            <description>Authors: Deng H, Jiang Q, Yang Y, Zhang S, Ma Y, Xie G, Chen X, Qian Z, Wen Y, Li J, Yang J, Chen L, Zhao X, Wei Y
    Polo-like kinase 1 (Plk1) is a key cell cycle regulator that is frequently overexpressed in human hepatocellular carcinomas. Blockade of the Plk1 pathway has been reported to be capable of inducing anti-tumor effect. Here, plasmids containing U6 promoter-driven shRNAs against human Plk1 were constructed and transfected in human hepatocellular carcinoma cell line HepG2. ShRNA targeting Plk1 almost completely reduced Plk1 expression in HepG2 hepatocellular carcinoma cells, as confirmed by RT-PCR and Western blot. As a consequence, HepG2 cells exhibited reduced proliferation and enhanced apoptosis in vitro. Most importantly, Treatment with Plk shRNA-DOTAP:Chol complex signifi...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350705</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:27 +0100</pubDate>
            <guid isPermaLink="false">4350705</guid>        </item>
        <item>
            <title>Caveolin-1 and mitochondrial SOD2 (MnSOD) function as tumor suppressors in the stromal microenvironment: A new genetically tractable model for human cancer associated fibroblasts.</title>
            <link>http://www.medworm.com/index.php?rid=4350704&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21150282%26dopt%3DAbstract</link>
            <description>Authors: Trimmer C, Sotgia F, Whitaker-Menezes D, Balliet R, Eaton G, Martinez-Outschoorn UE, Pavlides S, Howell A, Iozzo RV, Pestell RG, Scherer PE, Capozza F, Lisanti MP
    We have recently proposed a new model for understanding tumor metabolism, termed: &quot;The Autophagic Tumor Stroma Model of Cancer Metabolism&quot;. In this new paradigm, catabolism (autophagy) in the tumor stroma fuels the anabolic growth of aggressive cancer cells. Mechanistically, tumor cells induce autophagy in adjacent cancer-associated fibroblasts via the loss of caveolin-1 (Cav-1), which is sufficient to promote oxidative stress in stromal fibroblasts. To further test this hypothesis, here we created human Cav-1 deficient immortalized fibroblasts using a targeted sh-RNA knock-down approach. Relative to control fibrobla...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350704</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:23 +0100</pubDate>
            <guid isPermaLink="false">4350704</guid>        </item>
        <item>
            <title>ERG oncogene modulates prostaglandin signaling in prostate cancer cells.</title>
            <link>http://www.medworm.com/index.php?rid=4350703&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21178489%26dopt%3DAbstract</link>
            <description>This study suggests that ERG activation plays a role in prostaglandin signaling because knockdown of ERG expression in TMPRSS2-ERG fusion containing CaP cells leads to altered levels of the 15-hydroxy-prostaglandin dehydrogenase (HPGD), a tumor suppressor and prostaglandin catabolizing enzyme, and prostaglandin E2 (PGE2) . We demonstrate that HPGD expression is regulated by the binding of the ERG protein to the core promoter of this gene. Moreover, prostaglandin E2 dependent cell growth and urokinase-type plasminogen activator (uPA) expression are also affected by ERG knockdown. Together, these data imply that the ERG oncoprotein in CaP cells positively influence prostaglandin mediated signaling, which may contribute to tumor progression.
    PMID: 21178489 [PubMed - as supplied by publish...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350703</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:19 +0100</pubDate>
            <guid isPermaLink="false">4350703</guid>        </item>
        <item>
            <title>BMP-2 inhibits the tumorigenicity of cancer stem cells in human osteosarcoma OS99-1 cell line.</title>
            <link>http://www.medworm.com/index.php?rid=4350702&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21178508%26dopt%3DAbstract</link>
            <description>In this study, we evaluate the impact of BMP-2 on CSCs.Three types of BMP receptors were expressed in freshly sorted ALDHbr cells. In vitro, growth of the sorted ALDHbr cells was inhibited by BMP-2. Using RT-PCR analysis, BMP-2 was found to down-regulate the expression of embryonic stem cell markers Oct3/4, Nanog, and Sox-2, and up-regulate the transcription of osteogenic markers Runx-2 and Collagen Type I. In vivo, all animals receiving ALDHbr cells treated with BMP-2 did not form significant tumors, while untreated ALDHbr cells developed large tumor masses in NOD/SCID mice. Immunostaining confirmed few Ki-67 positive cells were present in the sections of tumor containing ALDHbr cells treated with BMP-2. These results suggest that BMP-2 suppresses tumor growth by reducing the gene express...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350702</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:16 +0100</pubDate>
            <guid isPermaLink="false">4350702</guid>        </item>
        <item>
            <title>Detection of ERG gene rearrangements and PTEN deletions in unsuspected prostate cancer of the transition zone.</title>
            <link>http://www.medworm.com/index.php?rid=4350701&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21178509%26dopt%3DAbstract</link>
            <description>In conclusion, although TZ and peripheral zone tumors share similar molecular etiologies, they exhibit differences in the rates of ERG and PTEN aberrations. The differences of ERG and /or PTEN genetic aberrations in TZ tumors may point toward a subset of tumors with adverse behavior. Additional studies implementing ERG and PTEN tissue-based FISH assays in tumors of the TZ are warranted to substantiate the potential clinical value of these biomarkers in the management of men with incidental PCA.
    PMID: 21178509 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350701</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:12 +0100</pubDate>
            <guid isPermaLink="false">4350701</guid>        </item>
        <item>
            <title>A polymeric nanoparticle formulation of curcumin inhibits growth, clonogenicity and stem-like fraction in malignant brain tumors.</title>
            <link>http://www.medworm.com/index.php?rid=4350700&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21193839%26dopt%3DAbstract</link>
            <description>Authors: Lim KJ, Bisht S, Bar EE, Maitra A, Eberhart CG
    Curcumin is a polyphenolic compound derived from the Indian spice turmeric. We used nanoparticle-encapsulated curcumin to treat medulloblastoma and glioblastoma cells. This formulation caused a dose-dependent decrease in growth of multiple brain tumor cell cultures, including the embryonal tumor derived lines DAOY and D283Med, and the glioblastoma neurosphere lines HSR-GBM1 and JHH-GBM14. The reductions in viable cell mass observed were associated with a combination of G2/M arrest and apoptotic induction. Curcumin also significantly decreased anchorage-independent clonogenic growth and reduced the CD133-positive stem-like population. Down-regulation of the insulin-like growth factor pathway in DAOY medulloblastoma cells was observ...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350700</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:09 +0100</pubDate>
            <guid isPermaLink="false">4350700</guid>        </item>
        <item>
            <title>PDRG1, a novel tumor marker for multiple malignancies that is selectively regulated by genotoxic stress.</title>
            <link>http://www.medworm.com/index.php?rid=4350699&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21193842%26dopt%3DAbstract</link>
            <description>In this study, we further investigated stress regulation of PDRG1 and found it to be selectively regulated by agents that induce genotoxic stress (DNA damage). Using cancer profiling arrays, we also investigated PDRG1 expression in matching normal and tumor samples representing various malignancies and found its expression to be upregulated in multiple malignancies including cancers of the colon, rectum, ovary, lung, stomach, breast and uterus when compared to their respective matched normal tissues. Western blot and immunohistochemical analyses were also performed on select specimen sets of colon cancers and matching normal tissues and the results also indicated PDRG1 overexpression in tumors relative to normal tissues. To gain insight into the function of PDRG1, we performed PDRG1 knockd...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4350699</comments>
            <pubDate>Sat, 15 Jan 2011 18:00:05 +0100</pubDate>
            <guid isPermaLink="false">4350699</guid>        </item>
        <item>
            <title>Identification of a new MAGE-A10 antigenic peptide presented by HLA-A*0201 on tumor cells.</title>
            <link>http://www.medworm.com/index.php?rid=4254386&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21124073%26dopt%3DAbstract</link>
            <description>In this study, we predicted HLA-A*0201-restricted CTL epitope peptides of MAGE-A10, followed by peptide/HLA-A*0201 binding affinity and complex stability assays, and induced peptide-specific CTL immune responses. Of the selected three peptides (designated P1, P2 and P3), P1 (MAGE-A10310-318, SLLKFLAKV) could elicit peptide-specific CTLs both in vitro from HLA-A*0201-positive PBMCs and in HLA-A*0201/Kb transgenic mice. And, the induced CTLs could lyse MAGE-A10-expressing tumor cells in a HLA-A*0201-restricted fashion but not MAGE-A10-negative tumor cells. Our results demonstrate that the peptide MAGE-A10310-318 is a HLA-A*0201-restricted CTL epitope of MAGE-A10 and could serve as a target for therapeutic antitumoral vaccination.
    PMID: 21124073 [PubMed - as supplied by publisher] (Source...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4254386</comments>
            <pubDate>Tue, 14 Dec 2010 00:30:35 +0100</pubDate>
            <guid isPermaLink="false">4254386</guid>        </item>
        <item>
            <title>PIK3CA mutations and EGFR overexpression predict for lithium sensitivity in human breast epithelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=4254385&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21124076%26dopt%3DAbstract</link>
            <description>Authors: Higgins MJ, Beaver JA, Wong HY, Gustin JP, Lauring JD, Garay JP, Konishi H, Mohseni M, Wang GM, Cidado J, Jelovac D, Cosgrove DP, Tamaki A, Abukhdeir AM, Park BH
    A high frequency of somatic mutations has been found in breast cancers within the gene encoding the catalytic p110α subunit of PI3K, PIK3CA. Using isogenic human breast epithelial cells, we have previously demonstrated that oncogenic PIK3CA &quot;hotspot&quot; mutations predict for response to the toxic effects of lithium. However, other somatic genetic alterations occur within this pathway in breast cancers, and it is possible that these changes may also predict for lithium sensitivity. We overexpressed the epidermal growth factor receptor (EGFR) into the non-tumorigenic human breast epithelial cell line MCF-10A, and compared...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4254385</comments>
            <pubDate>Tue, 14 Dec 2010 00:30:27 +0100</pubDate>
            <guid isPermaLink="false">4254385</guid>        </item>
        <item>
            <title>BMSC enhance the survival of paclitaxel treated squamous cell carcinoma cells in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=4254384&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21127403%26dopt%3DAbstract</link>
            <description>In conclusion, BMSC increase HNSCC resistance to treatment with paclitaxel in vitro. Tumor-stroma interactions are critical components of tumor biology including tumor invasion and metastatic potential. Therefore particular attention must be paid to the complex tumor-stroma interactions to fully understand how tumor cells become chemoresistant.
    PMID: 21127403 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4254384</comments>
            <pubDate>Tue, 14 Dec 2010 00:30:20 +0100</pubDate>
            <guid isPermaLink="false">4254384</guid>        </item>
        <item>
            <title>Microtubule-targeting-compound PBOX-15 radiosensitizes cancer cells in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=4254383&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21131779%26dopt%3DAbstract</link>
            <description>Conclusions: This preliminary data identifies the potential of PBOX-15 as a novel radiosensitising agent for the management of solid tumours and eradication of hypoxic cells.
    PMID: 21131779 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4254383</comments>
            <pubDate>Tue, 14 Dec 2010 00:30:13 +0100</pubDate>
            <guid isPermaLink="false">4254383</guid>        </item>
        <item>
            <title>Chemo-resistant melanoma sensitized by tamoxifen to low dose curcumin treatment through induction of apoptosis and autophagy.</title>
            <link>http://www.medworm.com/index.php?rid=4203545&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21088500%26dopt%3DAbstract</link>
            <description>In this report we show that curcumin does induce apoptosis in A375 and the relatively resistant G361 malignant human melanoma cell lines at higher doses. Tamoxifen is an estrogen receptor (ER) blocker that is used for ER positive breast cancer treatment. Recently, tamoxifen has been shown to directly target the mitochondria. Given that curcumin is a pro oxidant and tamoxifen can act on mitochondria, we ask whether the combinatorial treatment could result in synergistic induction of apoptosis in chemo-resistant melanoma. Our results show a corresponding increase in phosphatidyl serine flipping, mitochondria depolarization and reactive oxygen species (ROS) generation by the combined treatment at lower doses. Interestingly, there was significant induction of autophagy along with apoptosis fol...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203545</comments>
            <pubDate>Sat, 27 Nov 2010 00:50:46 +0100</pubDate>
            <guid isPermaLink="false">4203545</guid>        </item>
        <item>
            <title>Differential inhibition of transmembrane 4 L six family member 5 (TM4SF5)-mediated tumorigenesis by TSAHC and sorafenib.</title>
            <link>http://www.medworm.com/index.php?rid=4203544&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21099346%26dopt%3DAbstract</link>
            <description>In this study, TSAHC and two derivatives showed similar antagonistic activities against TM4SF5-mediated signaling and multilayer growth in vitro and anti-tumorigenic activity even in early stages of TM4SF5-mediated tumor formation in nude mice. Meanwhile, sorafenib was only effective much later in tumorigenesis in vivo and affected in vitro proliferation in a TM4SF5-independent manner. Altogether, these observations suggest that TSAHC may be a promising anti-tumorigenic reagent, especially against TM4SF5-mediated hepatocarcinoma.
    PMID: 21099346 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203544</comments>
            <pubDate>Sat, 27 Nov 2010 00:50:42 +0100</pubDate>
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        <item>
            <title>Role of the pituitary tumor transforming gene 1 in the progression of hepatocellular carcinoma.</title>
            <link>http://www.medworm.com/index.php?rid=4203543&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21099350%26dopt%3DAbstract</link>
            <description>Authors: Liang M, Chen X, Liu W, Li S, Li C, Jiang L, Lv S
    In order to demonstrate the role of the pituitary tumor transforming gene 1 (PTTG1) in the development of hepatocellular carcinoma (HCC) and its value as a molecular target for cancer therapy, we analyzed the expression of PTTG1 mRNA and protein, and their relation to clinicopathological characteristics and basic fibroblast growth factor (bFGF) expression in HCC. It was observed that the level of PTTG1 mRNA and the positive rate of PTTG1 protein in cancerous tissues were significantly higher than that in adjacent non-cancerous tissues (both P.
    PMID: 21099350 [PubMed - as supplied by publisher] (Source: Cancer Biology and Therapy)</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203543</comments>
            <pubDate>Sat, 27 Nov 2010 00:50:32 +0100</pubDate>
            <guid isPermaLink="false">4203543</guid>        </item>
        <item>
            <title>TGFβ-dependent induction of Interleukin-11 and Interleukin-8 involves SMAD and p38 MAPK pathways in breast tumor models with varied bone metastases potential.</title>
            <link>http://www.medworm.com/index.php?rid=4203542&amp;cid=s_37752_6_f&amp;fid=37752&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21099351%26dopt%3DAbstract</link>
            <description>Authors: Gupta J, Robbins J, Jilling T, Seth P
    We have delineated TGFβ signaling pathways in the production of osteolytic factors interleukin-8 and interleukin-11 in breast cancer cells with different bone metastases potential. Bone seeking MDA-MB-231(hm) cells expressed higher levels of IL-11, but lower levels of IL-8 compared to MDA-MB-231 cells. MCF-7 cells (mainly osteoblastic) did not express IL-8 or IL-11; MDA-MB-468 cells (weakly metastatic) expressed IL-8, but not IL-11. The up-regulation of IL-11 and IL-8 was associated with the rapid activation of SMAD2/3 and p38 MAPK through the TGFβ/TGFβR system. Analysis of TGFβ receptors indicated that MCF-7 cells do not express TGFβRII, and MDA-MB-468 cells do not express SMAD4. Inactivation of SMAD4 or p38PMAPK gene via RNAi result...</description>
            <author>Cancer Biology and Therapy</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4203542</comments>
            <pubDate>Sat, 27 Nov 2010 00:50:23 +0100</pubDate>
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