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 <title>all Kornelia Polyak stories</title>
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 <title>Flier hails new, cooperative era in Harvard science</title>
 <link>http://harvardscience.harvard.edu/medicine-health/articles/flier-hails-new-cooperative-era-harvard-science</link>
 <description>&lt;!--paging_filter--&gt;&lt;p&gt;&lt;a title=&quot;&quot; href=&quot;http://www.hms.harvard.edu&quot;&gt;Harvard Medical School&lt;/a&gt; Dean &lt;a title=&quot;&quot; href=&quot;http://harvardscience.harvard.edu/node/1004&quot;&gt;Jeffrey Flier &lt;/a&gt;Friday evening issued a call for new approaches to advance the fight against disease, embracing cross-institutional collaborations at Harvard as a way to bring new thinking to old problems.&lt;/p&gt;&lt;p&gt;Flier, the keynote speaker at the Fourth Annual Tony and Shelly Malkin Stem Cell Symposium at the Harvard Club of Boston, said he has spent a lot of time in his first months as Harvard Medical School Dean thinking about how and why the School does business. As he has gone through this process, Flier said, he’s given thought to who people mean when they speak of “we” at the Medical School.&lt;/p&gt;&lt;p&gt;&lt;a href=&quot;http://harvardscience.harvard.edu/medicine-health/articles/flier-hails-new-cooperative-era-harvard-science&quot;&gt;read more&lt;/a&gt;&lt;/p&gt;</description>
 <pubDate>Mon, 05 Nov 2007 14:02:11 -0500</pubDate>
 <dc:creator>404132862</dc:creator>
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 <title>Study questions &#039;cancer stem cell&#039; hypothesis in breast cancer growth</title>
 <link>http://harvardscience.harvard.edu/medicine-health/articles/study-questions-cancer-stem-cell-hypothesis-breast-cancer-growth</link>
 <description>&lt;!--paging_filter--&gt;&lt;p&gt;A Dana-Farber Cancer Institute study challenges the hypothesis that &quot;cancer stem cells&quot; — a small number of self-renewing cells within a tumor — are responsible for breast cancer progression and recurrence, and that wiping out these cells alone could cure the disease.&lt;/p&gt;
&lt;p&gt;Instead, the scientists report in the March issue of Cancer Cell that they have identified two genetically distinct populations of cancer cells in samples of human breast tumors — one of the types being a cell recently proposed by other scientists to be a true breast cancer stem cell.&lt;/p&gt;
&lt;p&gt;&lt;a href=&quot;http://harvardscience.harvard.edu/medicine-health/articles/study-questions-cancer-stem-cell-hypothesis-breast-cancer-growth&quot;&gt;read more&lt;/a&gt;&lt;/p&gt;</description>
 <pubDate>Wed, 11 Jul 2007 09:27:17 -0400</pubDate>
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 <title>Subtle changes in normal genes implicated in breast cancer</title>
 <link>http://harvardscience.harvard.edu/medicine-health/articles/subtle-changes-normal-genes-implicated-breast-cancer</link>
 <description>&lt;!--paging_filter--&gt;&lt;p&gt;Scientists found that benign cells surrounding breast  cancers undergo epigenetic modifications. The altered gene  function causes the microenvironment cells to signal  proliferation and increased aggression in the breast tumor cells.
&lt;p&gt;Kornelia Polyak, M.D., Ph.D., is senior author of the paper, which  was posted as an advance online publication on the Nature  Genetics Web site. Min Hu, Ph.D., of Dana-Farber, is first author  of the paper.
&lt;p&gt;Polyak&#039;s team had shown hyperactivity in genes in the breast  milk  microenvironment, even when their DNA was  unaltered during cell reproduction. She suspected inheritance of  the &#039;methylation state&#039; of the  DNA. Gene activity can be  regulated by the chemical switch process methylation, and the  on-off pattern of methylation in a cell&#039;s genes is hereditary, even  when the DNA remains unchanged. This is an example of  epigenetic modification.
&lt;p&gt;Cancer is often associated with abnormal methylation of   DNA. Polyak&#039;s team, looking to obtain the methylation pattern of  a cell&#039;s entire genome, developed the method Methylation  Specific Digital Karyotyping (MSDK). Polyak and her colleague  profiled the entire genome in weeks, far less time than with  conventional methods.
&lt;p&gt;Using MSDK, the scientists tested epithelial and myoepithelial  cells lining cancerous breast ducts, and the surrounding cells,  known as stoma, including fibroblasts. They found that in all of  these cell types, gene expression was altered by epigenetic  methylation changes that were absent in normal breast tissue.&lt;/p&gt;
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 <pubDate>Mon, 26 Mar 2007 06:21:10 -0400</pubDate>
 <dc:creator>70652986</dc:creator>
 <guid isPermaLink="false">3672 at http://harvardscience.harvard.edu</guid>
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 <title>Breast cancers tied to brain survival</title>
 <link>http://harvardscience.harvard.edu/medicine-health/articles/breast-cancers-tied-brain-survival</link>
 <description>&lt;!--paging_filter--&gt;&lt;p&gt;A gene produces a protein that evidently protects cancer cells in the same way it shields brain cells from damage caused by diseases like Alzheimer&#039;s and strokes. &quot;The same substance can be doubly harmful to some people with invasive breast cancer because it protects the tumor cells from death,&quot; notes Kornelia Polyak, an assistant professor of medicine at Harvard Medical School. Fragments of this Janus-like protein, dubbed dermcidin or DCD, have also been found in the blood of people with cachexia, a muscle-wasting disease that afflicts some terminally ill cancer patients. Such revelations have excited a number of drug companies about the potential uses of DCD. Since Polyak and her colleagues published their findings in September 2003 in the Proceedings of the National Academy of Science, several drug companies have contacted them about the possibility of using DCD as a means of diagnosing invasive breast cancer, the most common form of the malignancy.&lt;/p&gt;
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 <pubDate>Mon, 26 Mar 2007 05:32:30 -0400</pubDate>
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