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<title>Medical Xpress: Ludwig Institute for Cancer Research in the news</title>
<link>http://medicalxpress.com/</link>
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<description>Medical Xpress provides the latest news from Ludwig Institute for Cancer Research</description>

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     <title>Mapping the embryonic epigenome</title>
   	 <description>A large, multi-institutional research team involved in the NIH Epigenome Roadmap Project has published a sweeping analysis in the current issue of the journal Cell of how genes are turned on and off to direct early human development. Led by Bing Ren of the Ludwig Institute for Cancer Research, Joseph Ecker of The Salk Institute for Biological Studies and James Thomson of the Morgridge Institute for Research, the scientists also describe novel genetic phenomena likely to play a pivotal role not only in the genesis of the embryo, but that of cancer as well. Their publicly available data, the result of more than four years of experimentation and analysis, will contribute significantly to virtually every subfield of the biomedical sciences.</description>
	  <link>http://medicalxpress.com/news/2013-05-embryonic-epigenome.html</link>
	 <category>Genetics</category>
	 <pubDate>Thu, 09 May 2013 16:18:29 EST</pubDate>
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     <title>New study reveals how tumor suppressor p53 shut down in metastatic melanoma</title>
   	 <description>Cancer cells are a problem for the body because they multiply recklessly, refuse to die and blithely metastasize to set up shop in places where they don't belong. One protein that keeps healthy cells from behaving this way is a tumor suppressor named p53. This protein stops potentially precancerous cells from dividing and induces suicide in those that are damaged beyond repair. Not surprisingly, p53's critical function is disrupted in most cancers.</description>
	  <link>http://medicalxpress.com/news/2013-04-reveals-tumor-suppressor-p53-metastatic.html</link>
	 <category>Cancer</category>
	 <pubDate>Thu, 25 Apr 2013 12:53:11 EST</pubDate>
	 <guid isPermaLink="false">news286113174</guid>
	 
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     <title>A hijacking of healthy cellular circuits</title>
   	 <description>Proteins that control cell growth are often mutated in cancer, and their aberrant signaling drives the wild proliferation of cells that gives rise to tumors. One such protein, the epidermal growth factor receptor (EGFR), fuels a wide variety of cancers—including a highly malignant brain cancer known as glioblastoma. Yet drugs devised to block its signaling tend to work only for a short while, until the cancer cells adapt to evade the therapy. So far, much of the research examining such drug resistance has focused on how mutations of other proteins in cancer cells allow them to resist drugs.</description>
	  <link>http://medicalxpress.com/news/2013-04-hijacking-healthy-cellular-circuits.html</link>
	 <category>Cancer</category>
	 <pubDate>Mon, 08 Apr 2013 16:26:19 EST</pubDate>
	 <guid isPermaLink="false">news284657171</guid>
	 
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     <title>Novel combination therapy shuts down escape route, killing glioblastoma tumor cells</title>
   	 <description>Glioblastoma, the most common and lethal form of brain tumor in adults, is challenging to treat because the tumors rapidly become resistant to therapy. As cancer researchers are learning more about the causes of tumor cell growth and drug resistance, they are discovering molecular pathways that might lead to new targeted therapies to potentially treat this deadly cancer.</description>
	  <link>http://medicalxpress.com/news/2013-02-combination-therapy-route-glioblastoma-tumor.html</link>
	 <category>Cancer</category>
	 <pubDate>Tue, 26 Feb 2013 13:29:15 EST</pubDate>
	 <guid isPermaLink="false">news281107744</guid>
	 
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     <title>Epigenetic marker 5hmC opens door to studying its role in developmental disorders and disease</title>
   	 <description>Nearly every cell in the human body carries a copy of the full human genome. So how is it that the cells that detect light in the human eye are so different from those of, say, the beating heart or the spleen?</description>
	  <link>http://medicalxpress.com/news/2013-02-epigenetic-marker-5hmc-door-role.html</link>
	 <category>Genetics</category>
	 <pubDate>Mon, 04 Feb 2013 16:08:27 EST</pubDate>
	 <guid isPermaLink="false">news279216417</guid>
	 
</item>
<item>
     <title>How the tilt of a cell-surface receptor prevents cancer</title>
   	 <description>Clear communication between cells is essential to every aspect of the body's internal function. But since cells can't talk, or send emails, how do they communicate?</description>
	  <link>http://medicalxpress.com/news/2013-01-tilt-cell-surface-receptor-cancer.html</link>
	 <category>Cancer</category>
	 <pubDate>Thu, 31 Jan 2013 11:18:33 EST</pubDate>
	 <guid isPermaLink="false">news278853501</guid>
	 
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     <title>Predictors of cancer disease progression improve patient selection for metastasis-directed therapy</title>
   	 <description>Tumor metastasis, the ability of cancer cells to migrate from their tissue of origin and colonize elsewhere in the body, accounts for over 90% of cancer deaths. When patients die from cancer, it is usually caused by distant metastases established by malignant cells that split off from the primary cancer and began growing in new settings.</description>
	  <link>http://medicalxpress.com/news/2012-12-predictors-cancer-disease-patient-metastasis-directed.html</link>
	 <category>Cancer</category>
	 <pubDate>Tue, 11 Dec 2012 09:14:36 EST</pubDate>
	 <guid isPermaLink="false">news274439666</guid>
	 
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     <title>Mouse model exposes a new type of T cell to target melanoma</title>
   	 <description>Cancers arise in the body all the time. Most are nipped in the bud by the immune response, not least by its T cells, which detect telltale molecular markers—or antigens—on cancer cells and destroy them before they grow into tumors. Cancer cells, for their part, evolve constantly to evade such assassination. Those that succeed become full-blown malignancies. Yet, given the right sort of help, the immune system can destroy even these entrenched tumors.</description>
	  <link>http://medicalxpress.com/news/2012-10-mouse-exposes-cell-melanoma.html</link>
	 <category>Cancer</category>
	 <pubDate>Wed, 24 Oct 2012 12:00:01 EST</pubDate>
	 <guid isPermaLink="false">news270298157</guid>
	 
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     <title>Study uncovers mechanism by which tumor suppressor MIG6 triggers cell suicide</title>
   	 <description>Death plays a big role in keeping things alive. Consider the tightly orchestrated suicide of cells—a phenomenon essential to everything from shaping an embryo to keeping it free of cancer later in life. When cells refuse to die, and instead multiply uncontrollably, they become what we call tumors. An intricate circuitry of biochemical reactions inside cells coordinates their self-sacrifice. Tracing that circuitry is, naturally, an important part of cancer research.</description>
	  <link>http://medicalxpress.com/news/2012-09-uncovers-mechanism-tumor-suppressor-mig6.html</link>
	 <category>Cancer</category>
	 <pubDate>Mon, 24 Sep 2012 09:41:26 EST</pubDate>
	 <guid isPermaLink="false">news267698476</guid>
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     <title>Modification of tumor suppressor affects sensitivity to potential GBM treatment</title>
   	 <description>Despite years of research, glioblastoma, the most common and deadly brain cancer in adults, continues to outsmart treatments targeted to inhibit tumor growth.</description>
	  <link>http://medicalxpress.com/news/2012-08-modification-tumor-suppressor-affects-sensitivity.html</link>
	 <category>Cancer</category>
	 <pubDate>Mon, 13 Aug 2012 16:12:10 EST</pubDate>
	 <guid isPermaLink="false">news264093122</guid>
	 
</item>
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     <title>Molecular switch identified that controls key cellular process</title>
   	 <description>The body has a built-in system known as autophagy, or 'self-eating,' that controls how cells live or die. Deregulation of autophagy is linked to the development of human diseases, including neural degeneration and cancer.</description>
	  <link>http://medicalxpress.com/news/2012-08-molecular-key-cellular.html</link>
	 <category>Medical research</category>
	 <pubDate>Wed, 01 Aug 2012 15:51:22 EST</pubDate>
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