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        <title>Molecular Oncology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Molecular Oncology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Molecular+Oncology&t=Molecular+Oncology&s=Search&f=source]]></link>
        <lastBuildDate>Mon, 15 Mar 2010 13:53:55 +0100</lastBuildDate>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=3130578&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001446%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130578</comments>
            <pubDate>Thu, 31 Dec 2009 13:47:32 +0100</pubDate>
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            <title>Up-regulated Proteins in the Fluid Bathing the Tumour Cell Microenvironment as Potential Serological Markers for Early Detection of Cancer of the Breast</title>
            <link>http://www.medworm.com/index.php?rid=3130585&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001409%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Breast cancer is by far the most common diagnosed form of cancer and the leading cause of cancer death in women today. Clinically useful biomarkers for early detection of breast cancer could lead to a significant reduction in mortality. Here we describe a detailed analysis using gel-based proteomics in combination with mass spectrometry and immunohistochemistry (IHC) of the tumour interstitial fluids (TIF) and normal interstitial fluids (NIF) collected from 69 prospective breast cancer patients. The goal of this study was to identify abundant cancer up-regulated proteins that are externalised by cells in the tumour microenvironment of most if not all these lesions. To this end, we applied a phased biomarker discovery research strategy to the analysis of these samples rather than ...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130585</comments>
            <pubDate>Fri, 04 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130585</guid>        </item>
        <item>
            <title>New specific molecular targets for radio-chemotherapy of rectal cancer</title>
            <link>http://www.medworm.com/index.php?rid=3130584&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001392%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Patients with locally advanced rectal cancer often receive preoperative radio-chemotherapy (RCT). The mechanisms of tumour response to radiotherapy are not understood. The aim of this study was to identify the effects of RCT on gene expression in rectal tumour and normal rectal tissue. For that purpose tissue samples from 21 patients with resectable adenocarcinomas were collected for use in whole genome-microarray based gene expression analysis. A factorial experimental design allowed us to determine the effect of RCT on tumour tissue alone by removing the effect of radiation on normal tissue. This resulted in 1327 differentially expressed genes in tumour tissue with p (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130584</comments>
            <pubDate>Fri, 27 Nov 2009 00:00:00 +0100</pubDate>
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        <item>
            <title>Contents of Molecular Oncology Volume 3</title>
            <link>http://www.medworm.com/index.php?rid=2960399&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001252%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960399</comments>
            <pubDate>Thu, 05 Nov 2009 13:48:49 +0100</pubDate>
            <guid isPermaLink="false">2960399</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2960384&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001173%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960384</comments>
            <pubDate>Thu, 05 Nov 2009 13:48:47 +0100</pubDate>
            <guid isPermaLink="false">2960384</guid>        </item>
        <item>
            <title>Targeted Therapies: The Rare Cancer Paradigm</title>
            <link>http://www.medworm.com/index.php?rid=3130582&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001318%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: This review analyzes the state of the art of targeted therapies for several tumors, starting from the paradigmatic example of Imatinib treatment in chronic myelogenous leukemia (CML). We discuss how rare tumors can be models for various mechanisms of receptor tyrosine kinase (RTK) activation, and provide the opportunity to develop new therapies also for more common cancer types. We discuss the activation of the downstream RTK effectors as further targets for therapies in colorectal cancer. Finally, we highlight how a novel multidimensional approach which adds an in silico dimension to the in vitro and in vivo approach, can predict clinical results. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130582</comments>
            <pubDate>Thu, 05 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130582</guid>        </item>
        <item>
            <title>The unified approach: Meeting the cancer challenges of the next decade</title>
            <link>http://www.medworm.com/index.php?rid=3130579&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001306%2Fabstract%3Frss%3Dyes</link>
            <description>Introducing the Presidential session, Julio E. Celis, chairman of the Policy Committee of ECCO and scientific director of the Institute of Cancer Biology at the Danish Cancer Society in Copenhagen, said that the main objective of the session was to provide a unified approach to cancer research in Europe. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130579</comments>
            <pubDate>Mon, 02 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130579</guid>        </item>
        <item>
            <title>The US comprehensive cancer centers in perspective</title>
            <link>http://www.medworm.com/index.php?rid=3130580&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001136%2Fabstract%3Frss%3Dyes</link>
            <description>The United States began its “war on cancer” with the National Cancer Act of 1971, which authorized the creation of a new kind of facility that would combine research, clinical work, community outreach, prevention strategies, and population studies. Today, there are 41 institutions across the country which have been designated Comprehensive Cancer Centers by the National Cancer Institute (NCI). (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130580</comments>
            <pubDate>Mon, 26 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130580</guid>        </item>
        <item>
            <title>Topoisomerase IIα-dependent induction of a persistent DNA damage response in response to transient etoposide exposure</title>
            <link>http://www.medworm.com/index.php?rid=3130583&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001124%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cytotoxicity of the topoisomerase II (topoII) poison etoposide has been ascribed to the persistent covalent trapping of topoII in DNA cleavage complexes that become lethal as cells replicate their DNA. However, short term etoposide treatment also leads to subsequent cell death, suggesting that the lesions that lead to cytotoxicity arise rapidly and prior to the onset DNA replication. In the present study 1h treatment with 25μM etoposide was highly toxic and initiated a double-stranded DNA damage response as reflected by the recruitment of ATM, MDC1 and DNA-PKcs to γH2AX foci. While most DNA breaks were rapidly repaired upon withdrawal of the etoposide treatment, the repair machinery remained engaged in foci for at least 24h following withdrawal. TopoII siRNA ablation showed the...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130583</comments>
            <pubDate>Fri, 16 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130583</guid>        </item>
        <item>
            <title>Benchmarking biology research organizations using a new, dedicated tool</title>
            <link>http://www.medworm.com/index.php?rid=3130581&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001112%2Fabstract%3Frss%3Dyes</link>
            <description>We present a benchmark tool for scientific research organizations where, contrary to existing models, the group leader is placed in a central position within the organization. We used it in a pilot benchmark study involving six research institutions. Our study shows that data collection and data comparison based on this new tool can be achieved. It proved possible to compare relative performance and organizational characteristics and to generate suggestions for improvement for most participants. However, strict definitions of the parameters used for the benchmark and a thorough insight into the organization of each of the benchmark partners is required to produce comparable data and draw firm conclusions. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3130581</comments>
            <pubDate>Mon, 05 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3130581</guid>        </item>
        <item>
            <title>Immunotherapy in the landscape of new targeted treatments for non-small cell lung cancer</title>
            <link>http://www.medworm.com/index.php?rid=2960392&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001100%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related death worldwide. Active immunotherapies and molecules targeting tyrosine kinase receptors both offer new avenues for the treatment of NSCLC. Furthermore, their combinations or their administration along with standard treatments enlarges the potential for clinical benefit. Moreover, the discovery of biomarkers predicting the response to these new therapies should allow a better selection of patients susceptible to optimally benefit from these treatments. In this paper, we review the most promising active immunotherapies, antibodies and small molecules in the context of NSCLC management, focusing on compounds in phase III clinical development. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960392</comments>
            <pubDate>Tue, 22 Sep 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960392</guid>        </item>
        <item>
            <title>Tailoring cancer therapy – Validating basic science with the ‘supertrial’</title>
            <link>http://www.medworm.com/index.php?rid=2960388&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001094%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: A paradigm shift in research culture is needed in order to set up the large ambitious trials needed to make personalised medicine a reality. Emma Wilkinson talks to the experts about the hurdles they face and what needs to change. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960388</comments>
            <pubDate>Fri, 28 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960388</guid>        </item>
        <item>
            <title>Personal Profiles</title>
            <link>http://www.medworm.com/index.php?rid=2960385&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001033%2Fabstract%3Frss%3Dyes</link>
            <description>An overview of Personal Profiles can be found at http://www.moloncol.org.  Anton Berns Director of Research, The Netherlands Cancer Institute. Professor of Experimental Genetics of Inherited Diseases, University of Amsterdam. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960385</comments>
            <pubDate>Fri, 07 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960385</guid>        </item>
        <item>
            <title>Molecular profiling and characterization of luminal-like and basal-like in vivo breast cancer xenograft models</title>
            <link>http://www.medworm.com/index.php?rid=2960397&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109001021%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The number of relevant and well-characterized cell lines and xenograft models for studying human breast cancer are few, and may represent a limitation for this field of research. With the aim of developing new breast cancer model systems for in vivo studies of hormone dependent and independent tumor growth, progression and invasion, and for in vivo experimental therapy studies, we collected primary mammary tumor specimens from patients, and implanted them in immunodeficient mice. Primary tumor tissue from 29 patients with breast cancer was implanted subcutaneously with matrigel in SCID mice, in the presence of continuous release of estradiol. The tumors were transferred into new animals when reaching a diameter of 15mm and engrafted tumors were harvested for morphological and mol...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960397</comments>
            <pubDate>Thu, 06 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960397</guid>        </item>
        <item>
            <title>Transcription factors down-stream of Ras as molecular indicators for targeting malignancies with oncolytic herpes virus</title>
            <link>http://www.medworm.com/index.php?rid=2960396&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS157478910900101X%2Fabstract%3Frss%3Dyes</link>
            <description>This study, therefore, for the first time documents permissiveness of lymphoma cells to oncolytic herpes viruses and introduces ELK as a suitable factor for predicting tumor susceptibility to these novel anticancer agents. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960396</comments>
            <pubDate>Wed, 05 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960396</guid>        </item>
        <item>
            <title>Transforming growth-interacting factor (TGIF) regulates proliferation and differentiation of human myeloid leukemia cells</title>
            <link>http://www.medworm.com/index.php?rid=2960395&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000878%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Transforming growth-interacting factor (TGIF) is a homeobox transcriptional repressor that has been implicated in holoprosencephaly and various types of cancer. TGIF is expressed in hematopoietic stem cells and modulates TGF-β and retinoic acid (RA) signaling, both of which play an important role in hematopoiesis. We recently reported that TGIF's levels correlate inversely with survival in patients with acute myelogenous leukemia. Here we present the first direct evidence of a role for TGIF in myelopoiesis. We used short hairpin RNA interference to define the effects of TGIF knockdown on proliferation and differentiation of myeloid leukemia-derived cell lines. Decreased TGIF expression resulted in reduced proliferation and differentiation and lower expression of CEBPβ, CEBPε, ...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960395</comments>
            <pubDate>Wed, 05 Aug 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960395</guid>        </item>
        <item>
            <title>Contents of Molecular Oncology Volume 3</title>
            <link>http://www.medworm.com/index.php?rid=2664740&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000969%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664740</comments>
            <pubDate>Fri, 31 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2664740</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2664731&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS157478910900091X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664731</comments>
            <pubDate>Fri, 31 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2664731</guid>        </item>
        <item>
            <title>Identification of c-Src tyrosine kinase substrates in platelet-derived growth factor receptor signaling</title>
            <link>http://www.medworm.com/index.php?rid=2960394&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000866%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: c-Src non-receptor tyrosine kinase is an important component of the platelet-derived growth factor (PDGF) receptor signaling pathway. c-Src has been shown to mediate the mitogenic response to PDGF in fibroblasts. However, the exact components of PDGF receptor signaling pathway mediated by c-Src remain unclear. Here, we used stable isotope labeling with amino acids in cell culture (SILAC) coupled with mass spectrometry to identify Src-family kinase substrates involved in PDGF signaling. Using SILAC, we were able to detect changes in tyrosine phosphorylation patterns of 43 potential c-Src kinase substrates in PDGF receptor signaling. This included 23 known c-Src kinase substrates, of which 16 proteins have known roles in PDGF signaling while the remaining 7 proteins have not previo...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960394</comments>
            <pubDate>Fri, 17 Jul 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960394</guid>        </item>
        <item>
            <title>Putting Europe on the scientific map</title>
            <link>http://www.medworm.com/index.php?rid=2960387&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000854%2Fabstract%3Frss%3Dyes</link>
            <description>The pursuit of excellence has been a dominant theme in the career of Fotis Kafatos, a distinguished malaria researcher, who is now taking his high standards forward in providing support for the very brightest young scientists in Europe, as part of his presidency of The European Research Council. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960387</comments>
            <pubDate>Mon, 13 Jul 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960387</guid>        </item>
        <item>
            <title>Re: Sam Loewenberg's article, “Cancer policy in the Obama administration”</title>
            <link>http://www.medworm.com/index.php?rid=2960389&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000842%2Fabstract%3Frss%3Dyes</link>
            <description>In order to make progress in cancer research in the coming years, it's important first to understand the greatest hurdles standing in the way of federal funding for cancer research. From a patient's perspective, the media, for one thing, does a very poor job of educating and serving the public about cancer issues. The media tends to cover cancer when it strikes a celebrity. The problem is that the coverage is all human interest, and sometimes assumes the character of a death watch. I heard a cable news anchor, who lost a sister-in-law to breast cancer, explains how her producers almost never wanted to do stories related to cancer unless a celebrity was involved. Thus, TV, radio, newspapers, and blogs all fail to focus on substantive issues in cancer research including the lack of funding f...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960389</comments>
            <pubDate>Mon, 06 Jul 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960389</guid>        </item>
        <item>
            <title>Ras/MAPK signaling from endomembranes</title>
            <link>http://www.medworm.com/index.php?rid=2664734&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000829%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Signal transduction along the Ras/MAPK pathway has been generally thought to take place at the plasma membrane. It is now evident that the plasma membrane is not the only platform capable of Ras/MAPK signal induction. Fusion of Ras with green fluorescent protein and the development of genetically encoded fluorescent probes for Ras activation have revealed signaling events on a variety of intracellular membranes including endosomes, the Golgi apparatus and the endoplasmic reticulum. Thus, the Ras/MAPK pathway is spatially compartmentalized within cells and this may afford greater complexity of signal output. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664734</comments>
            <pubDate>Wed, 01 Jul 2009 23:00:00 +0100</pubDate>
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        <item>
            <title>Endocytosis, signaling and cancer, much more than meets the eye</title>
            <link>http://www.medworm.com/index.php?rid=2664732&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000830%2Fabstract%3Frss%3Dyes</link>
            <description>Any encyclopedia definition of “Endocytosis” will include statements such as “eukaryotic cells use endocytosis to internalize plasma membrane, surface receptors and their bound ligands, nutrients, bacterial toxins, immunoglobulins, viruses, and various extracellular soluble molecules” (). In other words, the canonical view of endocytosis has, for a long time, been that of a process designed to bring nutrients and/or other types of molecules inside the cell and, at the same time, to regulate the composition of the plasma membrane. Of course, endocytosis does all of this, and more… much more. The approaches that are being used to define molecular and biological details of all these “mores” constitute the leitmotif that unites the contributions included in this thematic issue of...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664732</comments>
            <pubDate>Wed, 01 Jul 2009 23:00:00 +0100</pubDate>
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        <item>
            <title>Endocytosis and signalling: A meeting with mathematics</title>
            <link>http://www.medworm.com/index.php?rid=2664735&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000805%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Although endocytosis has traditionally been understood as a signal attenuation mechanism, an emerging view considers endocytosis as an integral part of signal propagation and processing. On the short time scale, trafficking of endocytic vesicles contributes to signal propagation from the surface to distant targets, with bi-directional communication between signalling and trafficking. Mathematical modelling helps combine the mechanistic, molecular knowledge with rigorous analysis of the complex output dynamics of endocytosis in time and space. Simulations reveal novel roles for endocytosis, including the control of cell polarity, enhancing the spatial signal propagation, and controlling the signal magnitudes, kinetics, and synchronization with stimulus dynamics. (Source: Molecular...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664735</comments>
            <pubDate>Sun, 28 Jun 2009 23:00:00 +0100</pubDate>
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        <item>
            <title>Endocytic proteins in the regulation of nuclear signaling, transcription and tumorigenesis</title>
            <link>http://www.medworm.com/index.php?rid=2664736&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000817%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Accumulating evidence argues that many proteins governing membrane sorting during endocytosis participate also in nuclear signaling and transcriptional regulation, mostly by modulating the activity of various nuclear factors. Some adaptors and accessory proteins acting in clathrin-mediated internalization, as well as endosomal sorting proteins can undergo nuclear translocation and affect gene expression directly, while for others the effects may be more indirect. Although it is often unclear to what extent the endocytic and nuclear functions are interrelated, several of such proteins are implicated in the regulation of cell proliferation and tumorigenesis, arguing that their dual-function nature may be of physiological importance. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664736</comments>
            <pubDate>Sun, 21 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2664736</guid>        </item>
        <item>
            <title>Endocytosis and spatial restriction of cell signaling</title>
            <link>http://www.medworm.com/index.php?rid=2664733&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000787%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Endocytosis and recycling are essential components of the wiring enabling cells to perceive extracellular signals and transduce them in a temporally and spatially controlled fashion, directly influencing not only the duration and intensity of the signaling output, but also their correct location. Here, we will discuss key experimental evidence that support how different internalization routes, the generation of diverse endomembrane platforms, and cycles of internalization and recycling ensure polarized compartmentalization of signals, regulating a number of physiological and pathologically-relevant processes in which the resolution of spatial information is vital for their execution. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664733</comments>
            <pubDate>Thu, 18 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2664733</guid>        </item>
        <item>
            <title>Autophagy in tumour suppression and promotion</title>
            <link>http://www.medworm.com/index.php?rid=2664739&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000799%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Autophagy, a well-described cellular mechanism for lysosomal degradation of cytoplasmic content, has emerged as a tumour suppression pathway. Recent evidence indicates that the tumour suppressor function of autophagy is mediated by scavenging of damaged oxidative organelles, thereby preventing accumulation of toxic oxygen radicals that would cause genome instability. Paradoxically, however, in some cases autophagy can also promote the survival of cancer cells once tumours have developed. This is attributed to the ability of autophagy to promote cell survival under conditions of poor nutrient supply, as often faced by solid tumours and metastasising cancer cells. In addition, autophagy is frequently upregulated in tumours as a response to therapy and may protect tumours against th...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664739</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2664739</guid>        </item>
        <item>
            <title>At the crossroads of polarity, proliferation and apoptosis: The use of Drosophila to unravel the multifaceted role of endocytosis in tumor suppression</title>
            <link>http://www.medworm.com/index.php?rid=2664738&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000763%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Endocytosis is an important regulator of cell–cell signaling and endocytic trafficking has been increasingly implicated in control of tumor suppression. Recent insights from Drosophila indicate that impairment of multiple trafficking steps which lead to receptor degradation can cause tumor formation in epithelial organs. These tumors are characterized by sustained activation of a number of mitogenic signaling pathways, and by subversion of epithelial polarity and the apoptotic response. Cooperation between such alterations, as well as tumor–host interactions, is also observed. The recapitulation of several hallmarks of human cancers in fly tumors provides a framework to understand the role of defective endocytosis in cancer. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664738</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2664738</guid>        </item>
        <item>
            <title>Endocytosis, asymmetric cell division, stem cells and cancer: Unus pro omnibus, omnes pro uno</title>
            <link>http://www.medworm.com/index.php?rid=2664737&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000775%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Carcinogenesis can be initiated in adult stem cells, suggesting that tumours arise as a consequence of stem-cell dysfunction. In the fruitfly, cancer arises in stem cells that fail to undergo asymmetric cell division. In flies and mammals, a specific regulation of the endocytic trafficking machinery allows stem cells to self-renew and generate the differentiating cells required to form and maintain mature organs. We review recent findings suggesting that an understanding of the relationship between endocytosis, asymmetric cell division, stem cells and cancer will be crucial to unravel the cell biological basis of tumourigenesis. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2664737</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2664737</guid>        </item>
        <item>
            <title>Cancer policy in the Obama administration</title>
            <link>http://www.medworm.com/index.php?rid=2960386&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS157478910900074X%2Fabstract%3Frss%3Dyes</link>
            <description>In his first address to a joint session of Congress, President Barack Obama said he would devote resources to find “a cure for cancer in our time.” While that may be political rhetoric, it signals a commitment, and specifically a dollar commitment, to research funding that had been missing in the Bush administration, where research budgets languished. Obama has promised to double research funding for cancer during his term. In his first budget, he proposed increasing cancer research funding to $6 billion, which is about a 15 percent increase over existing levels. It is unclear what will happen by the time Congress gets through with it, but it is a promising sign. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960386</comments>
            <pubDate>Mon, 15 Jun 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960386</guid>        </item>
        <item>
            <title>The role of protein synthesis in cell cycling and cancer</title>
            <link>http://www.medworm.com/index.php?rid=2960391&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000751%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Cell cycling and protein synthesis are both key physiological tasks for cancer cells. Here we present a model for how the elongation phase of protein synthesis, governed by elongation factor 2 and elongation factor 2 kinase, both modulates and responds to cell cycling. Within this framework we also discuss survivin, a protein with both pro-mitotic and anti-apoptotic roles whose persistence in the cell is tied to protein synthesis due to its short half-life. Finally, we provide a brief overview of efforts of cancer researchers to target EF2 and EF2 kinase. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960391</comments>
            <pubDate>Fri, 12 Jun 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960391</guid>        </item>
        <item>
            <title>Corrigendum to “Has the US Cancer Centre model been ‘successful’? Lessons for the European cancer community” [Mol. Oncol. 3 (2009) 192–203]</title>
            <link>http://www.medworm.com/index.php?rid=2960398&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000738%2Fabstract%3Frss%3Dyes</link>
            <description>An unfortunate error occurred in the acknowledgement given in the footnote on page 192. The correct acknowledgement should read:  This work was supported by European Cancer Research Managers Foundation and funded by a grant from WHO International Agency for Research into Cancer (IARC). The MS Excel macros used to perform the geographical analysis of the papers were written by Dr. Philip Roe. Prof. Grant Lewison, Evalumetrics and University College London, UK provided the analysis for Figures 2, 3 and 4. Part of this research was conducted whilst RS was at Cancer Research UK. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960398</comments>
            <pubDate>Mon, 08 Jun 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960398</guid>        </item>
        <item>
            <title>Review on early technology assessments of nanotechnologies in oncology</title>
            <link>http://www.medworm.com/index.php?rid=2960390&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000726%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Nanotechnology is expected to play an increasingly important role in the diagnostics, prognostics, and management of targeted cancer treatments. While papers have described promising results for nanotechnology in experimental settings, the translation of fundamental research into clinical applications has yet to be widely adopted. In future, policy makers will need to anticipate new developments for clinical implementation and introduce technology assessments. Here we present an overview of the literature on the technology assessments that have already been undertaken on early stage nanotechnology in cancer care, with particular emphasis placed on clinical efficacy, efficiency, logistics, patient-related features and technology dynamics.Owing to the current stage of development o...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960390</comments>
            <pubDate>Mon, 08 Jun 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960390</guid>        </item>
        <item>
            <title>Contents of Molecular Oncology Volume 3</title>
            <link>http://www.medworm.com/index.php?rid=2417561&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000672%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2417561</comments>
            <pubDate>Tue, 19 May 2009 14:41:02 +0100</pubDate>
            <guid isPermaLink="false">2417561</guid>        </item>
        <item>
            <title>Conference calendar</title>
            <link>http://www.medworm.com/index.php?rid=2417560&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000660%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2417560</comments>
            <pubDate>Tue, 19 May 2009 14:41:02 +0100</pubDate>
            <guid isPermaLink="false">2417560</guid>        </item>
        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2417555&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000593%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2417555</comments>
            <pubDate>Tue, 19 May 2009 14:40:55 +0100</pubDate>
            <guid isPermaLink="false">2417555</guid>        </item>
        <item>
            <title>Characterizing DNA methylation patterns in pancreatic cancer genome</title>
            <link>http://www.medworm.com/index.php?rid=2960393&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000325%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: We performed a global methylation profiling assay on 1505 CpG sites across 807 genes to characterize DNA methylation patterns in pancreatic cancer genome. We found 289 CpG sites that were differentially methylated in normal pancreas, pancreatic tumors and cancer cell lines. We identified 23 and 35 candidate genes that are regulated by hypermethylation and hypomethylation in pancreatic cancer, respectively. We also identified candidate methylation markers that alter the expression of genes critical to gemcitabine susceptibility in pancreatic cancer. These results indicate that aberrant DNA methylation is a frequent epigenetic event in pancreatic cancer; and by using global methylation profiling assay, it is possible to identify these markers for diagnostic and therapeutic purposes...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2960393</comments>
            <pubDate>Fri, 08 May 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2960393</guid>        </item>
        <item>
            <title>Personal Profiles</title>
            <link>http://www.medworm.com/index.php?rid=2417556&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000556%2Fabstract%3Frss%3Dyes</link>
            <description>An overview of Personal Profiles can be found at http://www.moloncol.org.  Jiri Bartek (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2417556</comments>
            <pubDate>Wed, 22 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2417556</guid>        </item>
        <item>
            <title>An interview with Alexander Eggermont</title>
            <link>http://www.medworm.com/index.php?rid=2417557&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000490%2Fabstract%3Frss%3Dyes</link>
            <description>Taking a “helicopter view of oncology” has become the main role of Alexander Eggermont, the first president of the newly reformed European CanCer Organisation (ECCO), who is the driving force behind a new initiative to provide European governments with a “rationale” voice on oncology. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2417557</comments>
            <pubDate>Mon, 20 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2417557</guid>        </item>
        <item>
            <title>Full sequencing of TP53 identifies identical mutations within in situ and invasive components in breast cancer suggesting clonal evolution</title>
            <link>http://www.medworm.com/index.php?rid=2417559&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000489%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: In breast cancer, previous studies have suggested that somatic TP53 mutations are likely to be an early event. However, there are controversies regarding the cellular origin and linear course of breast cancer. The purpose of this study was to investigate tumor evolution in breast cancer by analyzing TP53 mutation status in tumors from various stages of the disease. The entire coding sequence of TP53 was sequenced in a cohort of pure ductal carcinoma in situ (DCIS), pure invasive cancer (≤15mm) and mixed lesions (i.e. invasive cancer with an in situ component). Of 118 tumor samples, 19 were found to harbor a TP53 mutation; 5 (15.6%) of the pure DCIS, 4 (10.5%) of the pure invasive cancers and 10 (20.8%) of the mixed lesions. In the mixed lesions, both the invasive and the DCIS c...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2417559</comments>
            <pubDate>Fri, 17 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2417559</guid>        </item>
        <item>
            <title>Has the US Cancer Centre model been ‘successful’? Lessons for the European cancer community</title>
            <link>http://www.medworm.com/index.php?rid=2417558&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000477%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The US model of Cancer Centres created by the National Cancer Act in 1971 has been one of the most tried and tested models of organised disease-specific scientific endeavors in the world. With many countries, particularly those in Europe now looking to develop the research arms of their National Cancer Control Programmes through the development of similar Cancer Centres the time is correct to consider the success and limitations of the US effort to date. Here we described the salient features of both US Cancer Centres and Networks, including their funding and evaluation with socio-political analysis on the learning points for Europe. In particular we highlight issues around sustainable funding, training and network development. New data highlighting deficiencies in the US model a...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2417558</comments>
            <pubDate>Mon, 06 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2417558</guid>        </item>
        <item>
            <title>Contents of Molecular Oncology Volume 3</title>
            <link>http://www.medworm.com/index.php?rid=2365872&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000441%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365872</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365872</guid>        </item>
        <item>
            <title>Conference calendar</title>
            <link>http://www.medworm.com/index.php?rid=2365871&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS157478910900043X%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365871</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365871</guid>        </item>
        <item>
            <title>Role of genetic polymorphisms and ovarian cancer susceptibility</title>
            <link>http://www.medworm.com/index.php?rid=2365870&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000246%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The value of identifying women with an inherited predisposition to epithelial ovarian cancer has become readily apparent with the identification of the BRCA1, and BRCA2 genes. Women who inherit a deleterious mutation in either of these genes have a very high lifetime risk of ovarian cancer (10–60%) and to some extent, increased risks of fallopian tube and peritoneal cancer. These highly lethal cancers are almost completely prevented by prophylactic salpingoophorectomy. BRCA1/2 mutation testing has become the accepted standard of care in families with a strong history of breast and/or ovarian cancer. This approach has the potential to reduce ovarian cancer mortality by about 10%.Although the ability to perform genetic testing for BRCA1 and 2 represents a significant clinical adv...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365870</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365870</guid>        </item>
        <item>
            <title>Intercepting pelvic cancer in the distal fallopian tube: Theories and realities</title>
            <link>http://www.medworm.com/index.php?rid=2365869&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000209%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The pathogenesis of high-grade serous carcinoma of the ovary has come into sharper focus as closer attention has been paid to the earlier phases of this disease. The study of patients with BRCA mutation has been of particular value, in as much as the examination of prophylactic salpingo-oophorectomies will reveal an early cancer in approximately 5% of individuals. Recently studies have shown that about 80% of these early carcinomas originate in the distal fallopian tube. This review summarizes the recent data supporting the distal fallopian tube as an important site for serous carcinogenesis, stressing both the presence of a novel precursor (the p53 signature) and the application of this model to all women irrespective of BRCA status. The challenges and unmet needs unmasked by th...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365869</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365869</guid>        </item>
        <item>
            <title>Large-scale genomic analysis of ovarian carcinomas</title>
            <link>http://www.medworm.com/index.php?rid=2365868&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789108001531%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Epithelial ovarian cancers are typified by frequent genomic aberrations that have been difficult to unravel. Recently, high-resolution array technologies have provided the first glimpse of the remarkable complexity of these aberrations with some ovarian cancers containing hundreds of copy number breakpoints, micro-deletions and amplifications. Many of these alterations contain cancer-related genes suggesting that the majority is disease-associated and not just the product of random genomic instability. Future developments such as next-generation sequencing and integrated analysis of data from multiple array platforms on large numbers of samples are poised to revolutionise our understanding of this complex disease. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365868</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365868</guid>        </item>
        <item>
            <title>Molecular profiles of hereditary epithelial ovarian cancers and their implications for the biology of this disease</title>
            <link>http://www.medworm.com/index.php?rid=2365867&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000179%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: BRCA1 and BRCA2 germline mutations account for the majority of hereditary ovarian cancers and comprise 10% of total cases. Ovarian cancers arising from these mutations exhibit both overlapping and distinct clinical and molecular features. The expression profiles of sporadic ovarian cancers show similarities to those of BRCA1 and BRCA2-related tumors suggesting that BRCA-related pathways may be involved in their development as well. The purpose of this review is to consider the available data on ovarian cancers in the context of other investigations of BRCA-related transcriptional alterations, and highlight areas for future research. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365867</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365867</guid>        </item>
        <item>
            <title>The Contribution of BRCA1 and BRCA2 to Ovarian Cancer</title>
            <link>http://www.medworm.com/index.php?rid=2365866&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000271%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Germline mutations of the BRCA1 and BRCA2 genes confer a high life-time risk of ovarian cancer. They represent the most significant and well characterised genetic risk factors so far identified for the disease. The frequency with which BRCA1/2 mutations occur in families containing multiple cases of ovarian cancer or breast and ovarian cancer, and in population-based ovarian cancer series varies geographically and between different ethnic groups. There are differences in the frequency of common mutations and in the presence of specific founder mutations in different populations. BRCA1 and BRCA2 are responsible for half of all families containing two or more ovarian cancer cases. In population-based studies, BRCA1 and BRCA2 mutations are present in 5–15% of all ovarian cancer ca...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365866</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365866</guid>        </item>
        <item>
            <title>Hereditary ovarian carcinoma: Heterogeneity, molecular genetics, pathology, and management</title>
            <link>http://www.medworm.com/index.php?rid=2365865&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000295%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Hereditary ovarian cancer accounts for at least 5% of the estimated 22,000 new cases of this disease during 2009. During this same time, over 15,000 will die from malignancy ascribed to ovarian origin. The bulk of these hereditary cases fits the hereditary breast–ovarian cancer syndrome, while virtually all of the remainder will be consonant with the Lynch syndrome, disorders which are autosomal dominantly inherited. Advances in molecular genetics have led to the identification of BRCA1 and BRCA2 gene mutations which predispose to the hereditary breast–ovarian cancer syndrome, and mutations in mismatch repair genes, the most common of which are MSH2 and MLH1, which predispose to Lynch syndrome. These discoveries enable relatively certain diagnosis, limited only by their varia...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
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            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Thematic issue on the molecular biology of hereditary ovarian cancer</title>
            <link>http://www.medworm.com/index.php?rid=2365864&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000301%2Fabstract%3Frss%3Dyes</link>
            <description>Ovarian cancer is a complex heterogeneous disease defined by histopathology, somatic molecular genetic attributes, and hereditary context. About 90% of ovarian cancers are of the epithelial type and within this group an estimated 5% are attributed to the inheritance of a highly penetrant allele that confers a significant life-time risk for developing ovarian cancer. In most developed countries, epithelial ovarian cancer is the fifth most common cause of death and is the most lethal form of gynecologic malignancy. Regardless of hereditary context, most cases are diagnosed at an advanced disease stage, where it has spread to other pelvic organs. Management is usually by surgical cytoreduction followed by platinum-based and taxane-based chemotherapy. Advanced disease is effectively managed in...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365864</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>The Bayh–Dole Act: A model for promoting research translation?</title>
            <link>http://www.medworm.com/index.php?rid=2365863&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789108001555%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: The Bayh-Dole Act of 1980 was passed with the intention of promoting research into cancer and other diseases by providing institutions and researchers with a commercial incentive, even though much of their work was publicly funded. Now, many are questioning whether the system has worked as promised and some warn it may be jeopardizing the pursuit of science with no direct market relevance. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365863</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Profile: Professor John Mendelsohn</title>
            <link>http://www.medworm.com/index.php?rid=2365862&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000283%2Fabstract%3Frss%3Dyes</link>
            <description>Lessons learnt from Hurricane Ike last autumn are now guiding John Mendelsohn in his management of the largest US cancer institute in the current financial down turn. “We face critical financial pressures due to decreasing federal research support, cutbacks in Medicaid and Medicare, reduced philanthropic gifts, and increases in expenses for medically indigent patients,” says Mendelsohn, president of the University of Texas M. D. Anderson Cancer Center. “We weathered the hurricane well, based on careful preparation and a spirit of dedication and teamwork when the storm arrived. It's in the same spirit we're planning to come through the adverse circumstances the nation now faces.” (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365862</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Thematic Issues</title>
            <link>http://www.medworm.com/index.php?rid=2365861&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000234%2Fabstract%3Frss%3Dyes</link>
            <description>Beginning with this issue Molecular Oncology introduces a new type of publication – Thematic Issues – that are intended to highlight a particular area of cancer research and to give an overview of where that specific field stands today and where it is heading to in the near future. The rational for introducing this new type of publication was prompted largely by the staggering expansion both in knowledge and technology in various areas of cancer research. These developments call for a forum in which new discoveries and future perspectives are integrated and presented in a timely manner. (Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365861</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
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        <item>
            <title>Editorial Board</title>
            <link>http://www.medworm.com/index.php?rid=2365860&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000362%2Fabstract%3Frss%3Dyes</link>
            <description>(Source: Molecular Oncology)</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2365860</comments>
            <pubDate>Wed, 01 Apr 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2365860</guid>        </item>
        <item>
            <title>Ectopic expression of plasma membrane targeted subunits of the Ndc80-complex as a tool to study kinetochore biochemistry</title>
            <link>http://www.medworm.com/index.php?rid=2486108&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000313%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Genomic stability depends on the normal function of the kinetochore, a multi-protein assemblage, which consists of over 80 molecules including both constitutive and transiently binding components. Information regarding the spatial–temporal assembly of kinetochore subcomplexes is often limited by technical difficulties in their isolation. To study kinetochore subcomplex formation, we targeted separately Hec1 and Spc24, two subunits of the Ndc80 kinetochore compilation, to the plasma membrane by fusing them with the amino-terminal palmitoylation and myristoylation (pm) sequence of the receptor tyrosine kinase Fyn. We found that in early mitotic cells, pm-GFP–Hec1 and pm-GFP–Spc24 fusion proteins localised to the plasma membrane and were able to recruit all subunits of the Ndc...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2486108</comments>
            <pubDate>Thu, 05 Mar 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2486108</guid>        </item>
        <item>
            <title>Discovery of epitopes for targeting the human epidermal growth factor receptor 2 (HER2) with antibodies</title>
            <link>http://www.medworm.com/index.php?rid=2486106&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000192%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Antibodies have become valuable therapeutic agents for targeting of extracellular proteins in various diseases, including cancer, autoimmunity and cardiovascular disorders. For breast cancer, antibodies targeting the human HER2 have been shown to result in cell growth inhibition both in vitro and in patients with breast tumors. There is evidence to suggest that targeting multiple HER2 epitopes may result in increased growth inhibition making it interesting to find antibodies targeting new epitopes. Here, we report on a new scheme to discover antibodies directed to new epitopes using the extracellular domain of the HER2 as a model. Polyclonal antibodies were generated using recombinant protein fragments and affinity purified fractions of the antibodies were functionally characteri...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2486106</comments>
            <pubDate>Fri, 13 Feb 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2486106</guid>        </item>
        <item>
            <title>Molecular characterization of apocrine carcinoma of the breast: Validation of an apocrine protein signature in a well-defined cohort</title>
            <link>http://www.medworm.com/index.php?rid=2486105&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000210%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Invasive apocrine carcinomas (IACs), as defined by morphological features, correspond to 0.3–4% of all invasive ductal carcinomas (IDC), and despite the fact that they are histologically distinct from other breast lesions there are currently no standard molecular criteria available for their diagnosis and no unequivocal information as to their prognosis. In an effort to address these concerns we have been using protein expression profiling technologies in combination with mass spectrometry and immunohistochemistry (IHC) to discover specific biomarkers that could allow us to molecularly characterize these lesions as well as to dissect some of the steps in the processes underlying breast apocrine metaplasia and development of precancerous apocrine lesions. Establishing these apoc...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2486105</comments>
            <pubDate>Fri, 13 Feb 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2486105</guid>        </item>
        <item>
            <title>Neurotensin signaling induces intracellular alkalinization and interleukin-8 expression in human pancreatic cancer cells</title>
            <link>http://www.medworm.com/index.php?rid=2486104&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000222%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: Pancreatic adenocarcinomas express neurotensin receptors in up to 90% of cases, however, their role in tumor biology and as a drug target is not clear. In the present study, a stable neurotensin (NT) analog induced intracellular calcium release and intracellular alkalinization in BxPC-3 and PANC-1 pancreatic cancer cells that was abolished by inhibitors of NT receptor (NTR) and sodium–proton exchanger 1 (NHE1), amiloride and SR 142948, respectively. Activation of NHE1 involved increased phosphorylation of dimethylfumarate-sensitive mitogen- and stress-activated kinase 1/2 (MSK1/2). NTR signaling appears to promote a metastatic phenotype in pancreatic cancer cells by induction of localized extracellular acidification in normoxic cells, preceeding acidosis induced by hypoxia and ...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2486104</comments>
            <pubDate>Thu, 12 Feb 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2486104</guid>        </item>
        <item>
            <title>Preclinical anticancer activity of the potent, oral Src inhibitor AZD0530</title>
            <link>http://www.medworm.com/index.php?rid=2486107&amp;cid=s_38555_6_f&amp;fid=38555&amp;url=http%3A%2F%2Fwww.moloncol.org%2Farticle%2FPIIS1574789109000180%2Fabstract%3Frss%3Dyes</link>
            <description>Abstract: AZD0530, an orally available Src inhibitor, demonstrated potent antimigratory and anti-invasive effects in vitro, and inhibited metastasis in a murine model of bladder cancer. Antiproliferative activity of AZD0530 in vitro varied between cell lines (IC50 0.2 –&gt;10μM). AZD0530 inhibited tumor growth in 4/10 xenograft models tested and dynamically inhibited in vivo phosphorylation of Src substrates paxillin and FAK in both growth-inhibition-resistant and -sensitive xenografts. The activity of AZD0530 in NBT-II bladder cancer cells in vitro was consistent with inhibition of cell migration and stabilization of cell–cell adhesion. These data suggest a dominant anti-invasive pharmacology for AZD0530 that may limit tumor progression in a range of cancers. AZD0530 is currently in Pha...</description>
            <author>Molecular Oncology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2486107</comments>
            <pubDate>Mon, 09 Feb 2009 00:00:00 +0100</pubDate>
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