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<title>Nature Reviews Cancer</title>
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<title>p53 — a Jack of all trades but master of none</title>
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<description>Cancers are rare because their evolution is actively restrained by a range of tumour suppressors. Of these p53 seems unusually crucial as either it or its attendant upstream or downstream pathways are inactivated in virtually all cancers. p53 is an evolutionarily ancient coordinator of metazoan </description>
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<p>
<b>p53 &#8212; a Jack of all trades but master of none</b>
</p>
<p>Nature Reviews Cancer 9, 821 (2009). <a href="http://dx.doi.org/10.1038/nrc2728">doi:10.1038/nrc2728</a>
</p>
<p>Authors: Melissa R. Junttila &amp; Gerard I. Evan</p>
<p>Cancers are rare because their evolution is actively restrained by a range of tumour suppressors. Of these p53 seems unusually crucial as either it or its attendant upstream or downstream pathways are inactivated in virtually all cancers. p53 is an evolutionarily ancient coordinator of metazoan </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/1rPNVyZnitU" height="1" width="1"/>]]></content:encoded>
<dc:title>p53 — a Jack of all trades but master of none</dc:title>
<dc:creator>Melissa R. Junttila</dc:creator>
<dc:creator>Gerard I. Evan</dc:creator>
<dc:identifier>doi:10.1038/nrc2728</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 821 (2009)</dc:source>
<dc:date>2009-09-24</dc:date>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
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<title>20 years studying p53 functions in genetically engineered mice</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/7Q7_qqWYxwU/nrc2731</link>
<description>Cell and molecular biological studies of p53 functions over the past 30 years have been complemented in the past 20 years by studies that use genetically engineered mice. As expected, mice that have mutant Trp53 alleles usually develop cancers of various types more rapidly </description>
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<p>
<b>20 years studying p53 functions in genetically engineered mice</b>
</p>
<p>Nature Reviews Cancer 9, 831 (2009). <a href="http://dx.doi.org/10.1038/nrc2731">doi:10.1038/nrc2731</a>
</p>
<p>Authors: Lawrence A. Donehower &amp; Guillermina Lozano</p>
<p>Cell and molecular biological studies of p53 functions over the past 30 years have been complemented in the past 20 years by studies that use genetically engineered mice. As expected, mice that have mutant Trp53 alleles usually develop cancers of various types more rapidly </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/7Q7_qqWYxwU" height="1" width="1"/>]]></content:encoded>
<dc:title>20 years studying p53 functions in genetically engineered mice</dc:title>
<dc:creator>Lawrence A. Donehower</dc:creator>
<dc:creator>Guillermina Lozano</dc:creator>
<dc:identifier>doi:10.1038/nrc2731</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 831 (2009)</dc:source>
<dc:date>2009-09-24</dc:date>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
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<item rdf:about="http://dx.doi.org/10.1038/nrc2751">
<title>Therapeutic resistance: Smoothing the way</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/-FY2YOhuRts/nrc2751</link>
<description>There is a compelling rationale for using hedgehog pathway inhibitors to treat both medulloblastoma and basal cell carcinoma. Phase I clinical trial data in basal cell carcinoma and a case study of a patient with medulloblastoma reported recently in the New England Journal of Medicine</description>
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<p>
<b>Therapeutic resistance: Smoothing the way</b>
</p>
<p>Nature Reviews Cancer 9, 768 (2009). <a href="http://dx.doi.org/10.1038/nrc2751">doi:10.1038/nrc2751</a>
</p>
<p>Author: Sarah Seton-Rogers</p>
<p>There is a compelling rationale for using hedgehog pathway inhibitors to treat both medulloblastoma and basal cell carcinoma. Phase I clinical trial data in basal cell carcinoma and a case study of a patient with medulloblastoma reported recently in the New England Journal of Medicine</p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/-FY2YOhuRts" height="1" width="1"/>]]></content:encoded>
<dc:title>Therapeutic resistance: Smoothing the way</dc:title>
<dc:creator>Sarah Seton-Rogers</dc:creator>
<dc:identifier>doi:10.1038/nrc2751</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 768 (2009)</dc:source>
<dc:date>2009-10-15</dc:date>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:publicationDate>2009-10-15</prism:publicationDate>
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<title>MicroRNA: Stage-specific signatures</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/XIRiMzYYl2Q/nrc2752</link>
<description>Do microRNA (miRNA) expression profiles reflect specific stages in tumour progression? Douglas Hanahan and colleagues set out to answer this question by analysing the miRNA transcriptome in distinct stages of tumorigenesis in the RIP1-Tag2 mouse model of pancreatic neuroendocrine tumours (PNETs).Normal, hyperplastic and </description>
<content:encoded><![CDATA[

<p>
<b>MicroRNA: Stage-specific signatures</b>
</p>
<p>Nature Reviews Cancer 9, 766 (2009). <a href="http://dx.doi.org/10.1038/nrc2752">doi:10.1038/nrc2752</a>
</p>
<p>Author: Sarah Seton-Rogers</p>
<p>Do microRNA (miRNA) expression profiles reflect specific stages in tumour progression? Douglas Hanahan and colleagues set out to answer this question by analysing the miRNA transcriptome in distinct stages of tumorigenesis in the RIP1-Tag2 mouse model of pancreatic neuroendocrine tumours (PNETs).Normal, hyperplastic and </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/XIRiMzYYl2Q" height="1" width="1"/>]]></content:encoded>
<dc:title>MicroRNA: Stage-specific signatures</dc:title>
<dc:creator>Sarah Seton-Rogers</dc:creator>
<dc:identifier>doi:10.1038/nrc2752</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 766 (2009)</dc:source>
<dc:date>2009-10-15</dc:date>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:publicationDate>2009-10-15</prism:publicationDate>
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<prism:number>11</prism:number>
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<title>Nanotechnology: Take a deep breath</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/YMtpK0s_1ss/nrc2753</link>
<description>The early detection of cancer is a priority for ensuring the best outcome for patients and reducing health care costs. The hunt is on for biomarkers that can identify individuals who are likely to have cancer, but inexpensive, simple and preferably minimally invasive methods of </description>
<content:encoded><![CDATA[

<p>
<b>Nanotechnology: Take a deep breath</b>
</p>
<p>Nature Reviews Cancer 9, 771 (2009). <a href="http://dx.doi.org/10.1038/nrc2753">doi:10.1038/nrc2753</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>The early detection of cancer is a priority for ensuring the best outcome for patients and reducing health care costs. The hunt is on for biomarkers that can identify individuals who are likely to have cancer, but inexpensive, simple and preferably minimally invasive methods of </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/YMtpK0s_1ss" height="1" width="1"/>]]></content:encoded>
<dc:title>Nanotechnology: Take a deep breath</dc:title>
<dc:creator>Nicola McCarthy</dc:creator>
<dc:identifier>doi:10.1038/nrc2753</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 771 (2009)</dc:source>
<dc:date>2009-10-15</dc:date>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:publicationDate>2009-10-15</prism:publicationDate>
<prism:doi>10.1038/nrc2753</prism:doi>
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<prism:volume>9</prism:volume>
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<prism:startingPage>771</prism:startingPage>
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<title>Therapy: Swings and roundabouts</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/awCPftNET0c/nrc2754</link>
<description>Children with neurofibromatosis type 1 are heterozygous for NF1 and have a substantially increased risk of developing an aggressive myeloproliferative disorder (MPD): juvenile myelomonocytic leukaemia (JMML). Using mouse models, Jennifer Lauchle, Kevin Shannon and colleagues have identified the stages of this disease that might </description>
<content:encoded><![CDATA[

<p>
<b>Therapy: Swings and roundabouts</b>
</p>
<p>Nature Reviews Cancer 9, 770 (2009). <a href="http://dx.doi.org/10.1038/nrc2754">doi:10.1038/nrc2754</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>Children with neurofibromatosis type 1 are heterozygous for NF1 and have a substantially increased risk of developing an aggressive myeloproliferative disorder (MPD): juvenile myelomonocytic leukaemia (JMML). Using mouse models, Jennifer Lauchle, Kevin Shannon and colleagues have identified the stages of this disease that might </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/awCPftNET0c" height="1" width="1"/>]]></content:encoded>
<dc:title>Therapy: Swings and roundabouts</dc:title>
<dc:creator>Nicola McCarthy</dc:creator>
<dc:identifier>doi:10.1038/nrc2754</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 770 (2009)</dc:source>
<dc:date>2009-10-15</dc:date>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:publicationDate>2009-10-15</prism:publicationDate>
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<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>770</prism:startingPage>
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<item rdf:about="http://dx.doi.org/10.1038/nrc2665-c1">
<title>Increase of wildlife cancer: an echo of plastic pollution?</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/_O0knyLb8lY/nrc2665-c1</link>
<description>The Science and Society article Wildlife cancer: a conservation perspective (Nature Rev. Cancer9, 517–526 (2009)) sparked our interest. Its authors McAloose and Newton noted that “in the marine environment, increases in spontaneous benign and malignant </description>
<content:encoded><![CDATA[

<p>
<b>Increase of wildlife cancer: an echo of plastic pollution?</b>
</p>
<p>Nature Reviews Cancer 9, 842 (2009). <a href="http://dx.doi.org/10.1038/nrc2665-c1">doi:10.1038/nrc2665-c1</a>
</p>
<p>Authors: Thomas Erren, Dominique Zeu&#223;, Frank Steffany &amp; Benno Meyer-Rochow</p>
<p>The Science and Society article Wildlife cancer: a conservation perspective (Nature Rev. Cancer9, 517&#8211;526 (2009)) sparked our interest. Its authors McAloose and Newton noted that &#8220;in the marine environment, increases in spontaneous benign and malignant </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/_O0knyLb8lY" height="1" width="1"/>]]></content:encoded>
<dc:title>Increase of wildlife cancer: an echo of plastic pollution?</dc:title>
<dc:creator>Thomas Erren</dc:creator>
<dc:creator>Dominique Zeuß</dc:creator>
<dc:creator>Frank Steffany</dc:creator>
<dc:creator>Benno Meyer-Rochow</dc:creator>
<dc:identifier>doi:10.1038/nrc2665-c1</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 842 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2665-c1</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2665-c1</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Correspondence</prism:section>
<prism:startingPage>842</prism:startingPage>
<prism:endingPage>842</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2665-c1</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2665-c2">
<title>Wildlife cancer and plastic pollution</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/u466PTYY2HY/nrc2665-c2</link>
<description>We would like to thank Thomas Erren, Dominique Zeuß, Frank Steffany, and Benno Meyer-Rochow for their thought-provoking comments on our Science and Society article (Wildlife cancer: a conservation perspective. Nature Rev. Cancer9, 517–526 (2009)). The information </description>
<content:encoded><![CDATA[

<p>
<b>Wildlife cancer and plastic pollution</b>
</p>
<p>Nature Reviews Cancer 9, 842 (2009). <a href="http://dx.doi.org/10.1038/nrc2665-c2">doi:10.1038/nrc2665-c2</a>
</p>
<p>Authors: Denise McAloose &amp; Alisa L. Newton</p>
<p>We would like to thank Thomas Erren, Dominique Zeu&#223;, Frank Steffany, and Benno Meyer-Rochow for their thought-provoking comments on our Science and Society article (Wildlife cancer: a conservation perspective. Nature Rev. Cancer9, 517&#8211;526 (2009)). The information </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/u466PTYY2HY" height="1" width="1"/>]]></content:encoded>
<dc:title>Wildlife cancer and plastic pollution</dc:title>
<dc:creator>Denise McAloose</dc:creator>
<dc:creator>Alisa L. Newton</dc:creator>
<dc:identifier>doi:10.1038/nrc2665-c2</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 842 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2665-c2</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2665-c2</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Correspondence</prism:section>
<prism:startingPage>842</prism:startingPage>
<prism:endingPage>842</prism:endingPage>
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<title>Emerging roles of E2Fs in cancer: an exit from cell cycle control</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/S1nWA8mlK5k/nrc2696</link>
<description>Mutations of the retinoblastoma tumour suppressor gene (RB1) or components regulating the RB pathway have been identified in almost every human malignancy. The E2F transcription factors function in cell cycle control and are intimately regulated by RB. Studies of model organisms have revealed </description>
<content:encoded><![CDATA[

<p>
<b>Emerging roles of E2Fs in cancer: an exit from cell cycle control</b>
</p>
<p>Nature Reviews Cancer 9, 785 (2009). <a href="http://dx.doi.org/10.1038/nrc2696">doi:10.1038/nrc2696</a>
</p>
<p>Authors: Hui-Zi Chen, Shih-Yin Tsai &amp; Gustavo Leone</p>
<p>Mutations of the retinoblastoma tumour suppressor gene (RB1) or components regulating the RB pathway have been identified in almost every human malignancy. The E2F transcription factors function in cell cycle control and are intimately regulated by RB. Studies of model organisms have revealed </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/S1nWA8mlK5k" height="1" width="1"/>]]></content:encoded>
<dc:title>Emerging roles of E2Fs in cancer: an exit from cell cycle control</dc:title>
<dc:creator>Hui-Zi Chen</dc:creator>
<dc:creator>Shih-Yin Tsai</dc:creator>
<dc:creator>Gustavo Leone</dc:creator>
<dc:identifier>doi:10.1038/nrc2696</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 785 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2696</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2696</prism:url>
<prism:volume>9</prism:volume>
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<prism:section>Review</prism:section>
<prism:startingPage>785</prism:startingPage>
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<title>STATs in cancer inflammation and immunity: a leading role for STAT3</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/LiRwK3V5toE/nrc2734</link>
<description>Commensurate with their roles in regulating cytokine-dependent inflammation and immunity, signal transducer and activator of transcription (STAT) proteins are central in determining whether immune responses in the tumour microenvironment promote or inhibit cancer. Persistently activated STAT3 and, to some extent, STAT5 increase tumour cell proliferation, </description>
<content:encoded><![CDATA[

<p>
<b>STATs in cancer inflammation and immunity: a leading role for STAT3</b>
</p>
<p>Nature Reviews Cancer 9, 798 (2009). <a href="http://dx.doi.org/10.1038/nrc2734">doi:10.1038/nrc2734</a>
</p>
<p>Authors: Hua Yu, Drew Pardoll &amp; Richard Jove</p>
<p>Commensurate with their roles in regulating cytokine-dependent inflammation and immunity, signal transducer and activator of transcription (STAT) proteins are central in determining whether immune responses in the tumour microenvironment promote or inhibit cancer. Persistently activated STAT3 and, to some extent, STAT5 increase tumour cell proliferation, </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/LiRwK3V5toE" height="1" width="1"/>]]></content:encoded>
<dc:title>STATs in cancer inflammation and immunity: a leading role for STAT3</dc:title>
<dc:creator>Hua Yu</dc:creator>
<dc:creator>Drew Pardoll</dc:creator>
<dc:creator>Richard Jove</dc:creator>
<dc:identifier>doi:10.1038/nrc2734</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 798 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2734</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2734</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Review</prism:section>
<prism:startingPage>798</prism:startingPage>
<prism:endingPage>809</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2734</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2735">
<title>NFAT proteins: emerging roles in cancer progression</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/mK0yEecG7M4/nrc2735</link>
<description>The roles of nuclear factor of activated T cells (NFAT) transcription factors have been extensively studied in the immune system. However, ubiquitous expression of NFAT isoforms in mammalian tissues has recently been observed, and a role for these transcription factors in human cancer is emerging. </description>
<content:encoded><![CDATA[

<p>
<b>NFAT proteins: emerging roles in cancer progression</b>
</p>
<p>Nature Reviews Cancer 9, 810 (2009). <a href="http://dx.doi.org/10.1038/nrc2735">doi:10.1038/nrc2735</a>
</p>
<p>Authors: Maria Mancini &amp; Alex Toker</p>
<p>The roles of nuclear factor of activated T cells (NFAT) transcription factors have been extensively studied in the immune system. However, ubiquitous expression of NFAT isoforms in mammalian tissues has recently been observed, and a role for these transcription factors in human cancer is emerging. </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/mK0yEecG7M4" height="1" width="1"/>]]></content:encoded>
<dc:title>NFAT proteins: emerging roles in cancer progression</dc:title>
<dc:creator>Maria Mancini</dc:creator>
<dc:creator>Alex Toker</dc:creator>
<dc:identifier>doi:10.1038/nrc2735</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 810 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2735</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2735</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Review</prism:section>
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<item rdf:about="http://dx.doi.org/10.1038/nrc2736">
<title>Polycomb group proteins: navigators of lineage pathways led astray in cancer</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/T-pIAVWQ2X0/nrc2736</link>
<description>The Polycomb group (PcG) proteins are transcriptional repressors that regulate lineage choices during development and differentiation. Recent studies have advanced our understanding of how the PcG proteins regulate cell fate decisions and how their deregulation potentially contributes to cancer. In this Review we discuss the </description>
<content:encoded><![CDATA[

<p>
<b>Polycomb group proteins: navigators of lineage pathways led astray in cancer</b>
</p>
<p>Nature Reviews Cancer 9, 773 (2009). <a href="http://dx.doi.org/10.1038/nrc2736">doi:10.1038/nrc2736</a>
</p>
<p>Authors: Adrian P. Bracken &amp; Kristian Helin</p>
<p>The Polycomb group (PcG) proteins are transcriptional repressors that regulate lineage choices during development and differentiation. Recent studies have advanced our understanding of how the PcG proteins regulate cell fate decisions and how their deregulation potentially contributes to cancer. In this Review we discuss the </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/T-pIAVWQ2X0" height="1" width="1"/>]]></content:encoded>
<dc:title>Polycomb group proteins: navigators of lineage pathways led astray in cancer</dc:title>
<dc:creator>Adrian P. Bracken</dc:creator>
<dc:creator>Kristian Helin</dc:creator>
<dc:identifier>doi:10.1038/nrc2736</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 773 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2736</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2736</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Review</prism:section>
<prism:startingPage>773</prism:startingPage>
<prism:endingPage>784</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2736</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2749">
<title>Genetics: An unanticipated role</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/pSgnY-wGRQM/nrc2749</link>
<description>Polycomb group (PcG) proteins silence differentiation genes during development and have been thought to have a primarily oncogenic role in human cancer. However, two studies in Drosophila melanogaster show that PcG proteins can also function as tumour suppressors by repressing key oncogenic signalling pathways.</description>
<content:encoded><![CDATA[

<p>
<b>Genetics: An unanticipated role</b>
</p>
<p>Nature Reviews Cancer 9, 765 (2009). <a href="http://dx.doi.org/10.1038/nrc2749">doi:10.1038/nrc2749</a>
</p>
<p>Author: Meera Swami</p>
<p>Polycomb group (PcG) proteins silence differentiation genes during development and have been thought to have a primarily oncogenic role in human cancer. However, two studies in Drosophila melanogaster show that PcG proteins can also function as tumour suppressors by repressing key oncogenic signalling pathways.</p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/pSgnY-wGRQM" height="1" width="1"/>]]></content:encoded>
<dc:title>Genetics: An unanticipated role</dc:title>
<dc:creator>Meera Swami</dc:creator>
<dc:identifier>doi:10.1038/nrc2749</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 765 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2749</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2749</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>765</prism:startingPage>
<prism:endingPage>765</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2749</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2750">
<title>Genetics: Becoming mobile</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/5qkS0qZaVtg/nrc2750</link>
<description>Mouse models have provided valuable insights into cancer biology, but have been limited in terms of performing unbiased genetic screens. Now an in vivo RNA interference screening approach has been used to identify determinants of lymphoma progression, showing that genes involved in cell motility </description>
<content:encoded><![CDATA[

<p>
<b>Genetics: Becoming mobile</b>
</p>
<p>Nature Reviews Cancer 9, 766 (2009). <a href="http://dx.doi.org/10.1038/nrc2750">doi:10.1038/nrc2750</a>
</p>
<p>Author: Meera Swami</p>
<p>Mouse models have provided valuable insights into cancer biology, but have been limited in terms of performing unbiased genetic screens. Now an in vivo RNA interference screening approach has been used to identify determinants of lymphoma progression, showing that genes involved in cell motility </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/5qkS0qZaVtg" height="1" width="1"/>]]></content:encoded>
<dc:title>Genetics: Becoming mobile</dc:title>
<dc:creator>Meera Swami</dc:creator>
<dc:identifier>doi:10.1038/nrc2750</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 766 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2750</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2750</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>766</prism:startingPage>
<prism:endingPage>767</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2750</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2755">
<title>Hypoxia: HIF1 in opposition</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/WdK9R_QCRvU/nrc2755</link>
<description>Constitutive expression of the hypoxia inducible factor 1 (HIF1) complex is most often associated with tumour progression and poor clinical outcome. However, expression of HIF1 is also evident during tumour suppression, and new results indicate that this might be the result of HIF1 regulation of </description>
<content:encoded><![CDATA[

<p>
<b>Hypoxia: HIF1 in opposition</b>
</p>
<p>Nature Reviews Cancer 9, 769 (2009). <a href="http://dx.doi.org/10.1038/nrc2755">doi:10.1038/nrc2755</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>Constitutive expression of the hypoxia inducible factor 1 (HIF1) complex is most often associated with tumour progression and poor clinical outcome. However, expression of HIF1 is also evident during tumour suppression, and new results indicate that this might be the result of HIF1 regulation of </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/WdK9R_QCRvU" height="1" width="1"/>]]></content:encoded>
<dc:title>Hypoxia: HIF1 in opposition</dc:title>
<dc:creator>Nicola McCarthy</dc:creator>
<dc:identifier>doi:10.1038/nrc2755</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 769 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2755</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2755</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>769</prism:startingPage>
<prism:endingPage>769</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2755</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2756">
<title>Genomics: We are individuals</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/6IepeqqWFfA/nrc2756</link>
<description>Improved sequencing technology has provided researchers with the tools to assess the genomic and transcriptomic landscape of tumour specimens at high resolution. The information gained from these mapping exercises could provide important insights into tumour-initiating events and how a tumour might evolve. Therefore, Marco Marra, </description>
<content:encoded><![CDATA[

<p>
<b>Genomics: We are individuals</b>
</p>
<p>Nature Reviews Cancer 9, 770 (2009). <a href="http://dx.doi.org/10.1038/nrc2756">doi:10.1038/nrc2756</a>
</p>
<p>Author: Gemma K. Alderton</p>
<p>Improved sequencing technology has provided researchers with the tools to assess the genomic and transcriptomic landscape of tumour specimens at high resolution. The information gained from these mapping exercises could provide important insights into tumour-initiating events and how a tumour might evolve. Therefore, Marco Marra, </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/6IepeqqWFfA" height="1" width="1"/>]]></content:encoded>
<dc:title>Genomics: We are individuals</dc:title>
<dc:creator>Gemma K. Alderton</dc:creator>
<dc:identifier>doi:10.1038/nrc2756</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 770 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2756</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2756</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>770</prism:startingPage>
<prism:endingPage>771</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2756</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2757">
<title>Cancer stem cells: Symmetry is key</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/GnI8N50gbv0/nrc2757</link>
<description>There is increasing evidence that the development and growth of many tumours is sustained by a small subset of cells, the cancer stem cells (CSCs). However, the characteristics that distinguish CSCs from normal stem cells (SCs) are largely undefined. In a paper recently published in </description>
<content:encoded><![CDATA[

<p>
<b>Cancer stem cells: Symmetry is key</b>
</p>
<p>Nature Reviews Cancer 9, 768 (2009). <a href="http://dx.doi.org/10.1038/nrc2757">doi:10.1038/nrc2757</a>
</p>
<p>Author: Mhairi Skinner</p>
<p>There is increasing evidence that the development and growth of many tumours is sustained by a small subset of cells, the cancer stem cells (CSCs). However, the characteristics that distinguish CSCs from normal stem cells (SCs) are largely undefined. In a paper recently published in </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/GnI8N50gbv0" height="1" width="1"/>]]></content:encoded>
<dc:title>Cancer stem cells: Symmetry is key</dc:title>
<dc:creator>Mhairi Skinner</dc:creator>
<dc:identifier>doi:10.1038/nrc2757</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 768 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2757</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2757</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>768</prism:startingPage>
<prism:endingPage>769</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2757</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2758">
<title>In Brief</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/WlCR8J5AXkk/nrc2758</link>
<description>Therapy</description>
<content:encoded><![CDATA[

<p>
<b>In Brief</b>
</p>
<p>Nature Reviews Cancer 9, 766 (2009). <a href="http://dx.doi.org/10.1038/nrc2758">doi:10.1038/nrc2758</a>
</p>
<p>Therapy</p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/WlCR8J5AXkk" height="1" width="1"/>]]></content:encoded>
<dc:title>In Brief</dc:title>
<dc:identifier>doi:10.1038/nrc2758</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 766 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2758</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2758</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>766</prism:startingPage>
<prism:endingPage>766</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2758</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2759">
<title>Trial watch</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/9TFf-bKWJcg/nrc2759</link>
<description>A double hitA Phase I/II safety and immunogenicity evaluation trial of trastuzumab combined with ERBB2 vaccination in patients with metastatic breast cancer has recently been published.Twenty-two patients with stage IV, ERBB2-positive breast cancer who were being treated with trastuzumab were vaccinated with an </description>
<content:encoded><![CDATA[

<p>
<b>Trial watch</b>
</p>
<p>Nature Reviews Cancer 9, 767 (2009). <a href="http://dx.doi.org/10.1038/nrc2759">doi:10.1038/nrc2759</a>
</p>
<p>A double hitA Phase I/II safety and immunogenicity evaluation trial of trastuzumab combined with ERBB2 vaccination in patients with metastatic breast cancer has recently been published.Twenty-two patients with stage IV, ERBB2-positive breast cancer who were being treated with trastuzumab were vaccinated with an </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/9TFf-bKWJcg" height="1" width="1"/>]]></content:encoded>
<dc:title>Trial watch</dc:title>
<dc:identifier>doi:10.1038/nrc2759</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 767 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2759</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2759</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>767</prism:startingPage>
<prism:endingPage>767</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2759</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2760">
<title>Emotionally stressed</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/NDF3yO_Ujm8/nrc2760</link>
<description>Breast cancer could be exacerbated by social isolation, a study in mice has suggested.Suzanne Conzen and colleagues at the University of Chicago, USA, raised mice that were genetically predisposed to developing breast cancer either in groups or isolated from the time that they were </description>
<content:encoded><![CDATA[

<p>
<b>Emotionally stressed</b>
</p>
<p>Nature Reviews Cancer 9, 770 (2009). <a href="http://dx.doi.org/10.1038/nrc2760">doi:10.1038/nrc2760</a>
</p>
<p>Author: Sarah Seton-Rogers</p>
<p>Breast cancer could be exacerbated by social isolation, a study in mice has suggested.Suzanne Conzen and colleagues at the University of Chicago, USA, raised mice that were genetically predisposed to developing breast cancer either in groups or isolated from the time that they were </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/NDF3yO_Ujm8" height="1" width="1"/>]]></content:encoded>
<dc:title>Emotionally stressed</dc:title>
<dc:creator>Sarah Seton-Rogers</dc:creator>
<dc:identifier>doi:10.1038/nrc2760</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 770 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2760</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2760</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>770</prism:startingPage>
<prism:endingPage>770</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2760</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2762">
<title>From the editors</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/OgGASGw89CQ/nrc2762</link>
<description>As one door closes, another opens, and so it is with two of our Article Series this month. The Review on page page 785 by Hui-Zi Chen, Shih-Yin Tsai and Gustavo Leone is the last in our short series on RB and E2F. In </description>
<content:encoded><![CDATA[

<p>
<b>From the editors</b>
</p>
<p>Nature Reviews Cancer 9, 763 (2009). <a href="http://dx.doi.org/10.1038/nrc2762">doi:10.1038/nrc2762</a>
</p>
<p>As one door closes, another opens, and so it is with two of our Article Series this month. The Review on page page 785 by Hui-Zi Chen, Shih-Yin Tsai and Gustavo Leone is the last in our short series on RB and E2F. In </p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/OgGASGw89CQ" height="1" width="1"/>]]></content:encoded>
<dc:title>From the editors</dc:title>
<dc:identifier>doi:10.1038/nrc2762</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 763 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:doi>10.1038/nrc2762</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2762</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>From The Editors</prism:section>
<prism:startingPage>763</prism:startingPage>
<prism:endingPage>763</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2762</feedburner:origLink></item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2683-c1">
<title>Genetic matters of CYP2D6 in breast cancer: copy number variations and nucleotide polymorphisms</title>
<link>http://feeds.nature.com/~r/nrc/rss/current/~3/TmdeU4Muxso/nrc2683-c1</link>
<description>We read with great interest the content-rich Review CYP2D6 and tamoxifen: DNA matters in breast cancer (CYP2D6</description>
<content:encoded><![CDATA[

<p>
<b>Genetic matters of CYP2D6 in breast cancer: copy number variations and nucleotide polymorphisms</b>
</p>
<p>Nature Reviews Cancer 9, 842 (2009). <a href="http://dx.doi.org/10.1038/nrc2683-c1">doi:10.1038/nrc2683-c1</a>
</p>
<p>Authors: Ke-Da Yu &amp; Zhi-Ming Shao</p>
<p>We read with great interest the content-rich Review CYP2D6 and tamoxifen: DNA matters in breast cancer (CYP2D6</p>
<img src="http://feeds.feedburner.com/~r/nrc/rss/current/~4/TmdeU4Muxso" height="1" width="1"/>]]></content:encoded>
<dc:title>Genetic matters of CYP2D6 in breast cancer: copy number variations and nucleotide polymorphisms</dc:title>
<dc:creator>Ke-Da Yu</dc:creator>
<dc:creator>Zhi-Ming Shao</dc:creator>
<dc:identifier>doi:10.1038/nrc2683-c1</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 842 (2009)</dc:source>
<dc:date>2009-10-23</dc:date>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:publicationDate>2009-10-23</prism:publicationDate>
<prism:doi>10.1038/nrc2683-c1</prism:doi>
<prism:url>http://dx.doi.org/10.1038/nrc2683-c1</prism:url>
<prism:volume>9</prism:volume>
<prism:number>11</prism:number>
<prism:section>Correspondence</prism:section>
<prism:startingPage>842</prism:startingPage>
<prism:endingPage>843</prism:endingPage>
<feedburner:origLink>http://dx.doi.org/10.1038/nrc2683-c1</feedburner:origLink></item>
</rdf:RDF>
