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<title>Breast cancer: Metastasis on the brain</title>
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<description>Breast cancer metastasis to the brain typically occurs after metastasis to other organs, possibly because the metastasizing cells must be capable of not only general extravasation but also of passing through the blood-brain barrier (BBB). Using gene expression analysis of breast cancer cells that exhibit </description>
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<b>Breast cancer: Metastasis on the brain</b>
</p>
<p>Nature Reviews Cancer 9, 460 (2009). <a href="http://dx.doi.org/10.1038/nrc2678">doi:10.1038/nrc2678</a>
</p>
<p>Author: Sarah Seton-Rogers</p>
<p>Breast cancer metastasis to the brain typically occurs after metastasis to other organs, possibly because the metastasizing cells must be capable of not only general extravasation but also of passing through the blood-brain barrier (BBB). Using gene expression analysis of breast cancer cells that exhibit </p>
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<title>Epigenetics: Misreading the code</title>
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<description>A new study has shown that the deregulation of histone methylation at loci that encode differentiation-specific transcription factors is oncogenic, suggesting that misinterpretation of the histone code could be an important mechanism in cancer.Plant homeodomain (PHD) fingers are evolutionarily conserved protein modules that recognize </description>
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<b>Epigenetics: Misreading the code</b>
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<p>Nature Reviews Cancer 9, 461 (2009). <a href="http://dx.doi.org/10.1038/nrc2679">doi:10.1038/nrc2679</a>
</p>
<p>Author: Meera Swami</p>
<p>A new study has shown that the deregulation of histone methylation at loci that encode differentiation-specific transcription factors is oncogenic, suggesting that misinterpretation of the histone code could be an important mechanism in cancer.Plant homeodomain (PHD) fingers are evolutionarily conserved protein modules that recognize </p>
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<title>Breast cancer: A DEAR 1</title>
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<description>Young women diagnosed with breast cancer tend to have a more aggressive disease than women diagnosed later in life. Discovering genes that lead to breast cancer in younger women is imperative if treatment is to improve. Ann McNeill Killary and colleagues have identified a potential </description>
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<p>
<b>Breast cancer: A DEAR 1</b>
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<p>Nature Reviews Cancer 9, 460 (2009). <a href="http://dx.doi.org/10.1038/nrc2680">doi:10.1038/nrc2680</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>Young women diagnosed with breast cancer tend to have a more aggressive disease than women diagnosed later in life. Discovering genes that lead to breast cancer in younger women is imperative if treatment is to improve. Ann McNeill Killary and colleagues have identified a potential </p>
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<title>Novel anticancer targets: revisiting ERBB2 and discovering ERBB3</title>
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<description>Aberrant receptor expression or functioning of the epidermal growth factor receptor (Erbb) family plays a crucial part in the development and evolution of cancer. Inhibiting the signalling activity of individual receptors in this family has advanced the treatment of a range of human cancers. In </description>
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<p>
<b>Novel anticancer targets: revisiting ERBB2 and discovering ERBB3</b>
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<p>Nature Reviews Cancer 9, 463 (2009). <a href="http://dx.doi.org/10.1038/nrc2656">doi:10.1038/nrc2656</a>
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<p>Authors: Jos&#233; Baselga &amp; Sandra M. Swain</p>
<p>Aberrant receptor expression or functioning of the epidermal growth factor receptor (Erbb) family plays a crucial part in the development and evolution of cancer. Inhibiting the signalling activity of individual receptors in this family has advanced the treatment of a range of human cancers. In </p>
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<dc:source>Nature Reviews Cancer 9, 463 (2009)</dc:source>
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<title>Genetic prognostic and predictive markers in colorectal cancer</title>
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<description>Despite many studies of the likely survival outcome of individual patients with colorectal cancer, our knowledge of this subject remains poor. Until recently, we had virtually no understanding of individual responses to therapy, but the discovery of the KRAS mutation as a marker of probable </description>
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<p>
<b>Genetic prognostic and predictive markers in colorectal cancer</b>
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<p>Nature Reviews Cancer 9, 489 (2009). <a href="http://dx.doi.org/10.1038/nrc2645">doi:10.1038/nrc2645</a>
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<p>Authors: Axel Walther, Elaine Johnstone, Charles Swanton, Rachel Midgley, Ian Tomlinson &amp; David Kerr</p>
<p>Despite many studies of the likely survival outcome of individual patients with colorectal cancer, our knowledge of this subject remains poor. Until recently, we had virtually no understanding of individual responses to therapy, but the discovery of the KRAS mutation as a marker of probable </p>
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<dc:source>Nature Reviews Cancer 9, 489 (2009)</dc:source>
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<title>Cancer prevention research &#8212; then and now</title>
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<description>Throughout history, humankind has won the battle against deadly diseases, including small pox and polio, by defeating them through prevention. Cancer prevention is a global priority, but studying history suggests that the journey towards achieving this goal is difficult and full of detours and roadblocks. </description>
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<p>
<b>Cancer prevention research &#8212; then and now</b>
</p>
<p>Nature Reviews Cancer 9, 508 (2009). <a href="http://dx.doi.org/10.1038/nrc2646">doi:10.1038/nrc2646</a>
</p>
<p>Authors: Ann M. Bode &amp; Zigang Dong</p>
<p>Throughout history, humankind has won the battle against deadly diseases, including small pox and polio, by defeating them through prevention. Cancer prevention is a global priority, but studying history suggests that the journey towards achieving this goal is difficult and full of detours and roadblocks. </p>
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<dc:title>Cancer prevention research &#8212; then and now</dc:title>
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<dc:source>Nature Reviews Cancer 9, 508 (2009)</dc:source>
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<description>In multicellular organisms, the total number of cells is a balance between the cell-generating effects of mitosis and cell death that is induced through apoptosis. A disruption of this delicate balance can lead to the development of cancer. This Timeline article focuses on how the </description>
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<p>
<b>Apoptosis and cancer: the genesis of a research field</b>
</p>
<p>Nature Reviews Cancer 9, 501 (2009). <a href="http://dx.doi.org/10.1038/nrc2663">doi:10.1038/nrc2663</a>
</p>
<p>Author: Thomas G. Cotter</p>
<p>In multicellular organisms, the total number of cells is a balance between the cell-generating effects of mitosis and cell death that is induced through apoptosis. A disruption of this delicate balance can lead to the development of cancer. This Timeline article focuses on how the </p>
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<dc:title>Apoptosis and cancer: the genesis of a research field</dc:title>
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<dc:source>Nature Reviews Cancer 9, 501 (2009)</dc:source>
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<title>Wildlife cancer: a conservation perspective</title>
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<description>Until recently, cancer in wildlife was not considered to be a conservation concern. However, with the identification of Tasmanian devil facial tumour disease, sea turtle fibropapillomatosis and sea lion genital carcinoma, it has become apparent that neoplasia can be highly prevalent and have considerable effects </description>
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<p>
<b>Wildlife cancer: a conservation perspective</b>
</p>
<p>Nature Reviews Cancer 9, 517 (2009). <a href="http://dx.doi.org/10.1038/nrc2665">doi:10.1038/nrc2665</a>
</p>
<p>Authors: Denise McAloose &amp; Alisa L. Newton</p>
<p>Until recently, cancer in wildlife was not considered to be a conservation concern. However, with the identification of Tasmanian devil facial tumour disease, sea turtle fibropapillomatosis and sea lion genital carcinoma, it has become apparent that neoplasia can be highly prevalent and have considerable effects </p>
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<dc:source>Nature Reviews Cancer 9, 517 (2009)</dc:source>
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<title>Chemoprevention of lung carcinogenesis in addicted smokers and ex-smokers</title>
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<description>Chemoprevention of lung carcinogenesis is one approach to controlling the epidemic of lung cancer caused by cigarette smoking. The target for chemoprevention should be the activities of the multiple carcinogens, toxicants, co-carcinogens, tumour promoters and inflammatory compounds in cigarette smoke. At present there are many </description>
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<p>
<b>Chemoprevention of lung carcinogenesis in addicted smokers and ex-smokers</b>
</p>
<p>Nature Reviews Cancer 9, 476 (2009). <a href="http://dx.doi.org/10.1038/nrc2674">doi:10.1038/nrc2674</a>
</p>
<p>Authors: Stephen S. Hecht, Fekadu Kassie &amp; Dorothy K. Hatsukami</p>
<p>Chemoprevention of lung carcinogenesis is one approach to controlling the epidemic of lung cancer caused by cigarette smoking. The target for chemoprevention should be the activities of the multiple carcinogens, toxicants, co-carcinogens, tumour promoters and inflammatory compounds in cigarette smoke. At present there are many </p>
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<dc:title>Chemoprevention of lung carcinogenesis in addicted smokers and ex-smokers</dc:title>
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<dc:identifier>doi:10.1038/nrc2674</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 476 (2009)</dc:source>
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<title>Breast cancer: Prioritizing targets</title>
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<description>A current priority in cancer research is to identify genetic alterations that are directly involved in tumorigenesis and develop therapies to target them. Arul Chinnaiyan and colleagues have used a prioritization strategy to show that angiotensin II receptor type I (AGTR1) is overexpressed </description>
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<p>
<b>Breast cancer: Prioritizing targets</b>
</p>
<p>Nature Reviews Cancer 9, 458 (2009). <a href="http://dx.doi.org/10.1038/nrc2684">doi:10.1038/nrc2684</a>
</p>
<p>Author: Meera Swami</p>
<p>A current priority in cancer research is to identify genetic alterations that are directly involved in tumorigenesis and develop therapies to target them. Arul Chinnaiyan and colleagues have used a prioritization strategy to show that angiotensin II receptor type I (AGTR1) is overexpressed </p>
]]></content:encoded>
<dc:title>Breast cancer: Prioritizing targets</dc:title>
<dc:creator>Meera Swami</dc:creator>
<dc:identifier>doi:10.1038/nrc2684</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 458 (2009)</dc:source>
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<title>Senescence: Playing games with epigenetics</title>
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<description>The CDKN2A locus encodes the tumour suppressors INK4A and ARF, which induce senescence through independent pathways. CDKN2A expression is repressed by histone H3 lysine 27 trimethylation (H3K27me3), which is mediated by polycomb group proteins. This repression is reversed in response to cellular stress, </description>
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<p>
<b>Senescence: Playing games with epigenetics</b>
</p>
<p>Nature Reviews Cancer 9, 456 (2009). <a href="http://dx.doi.org/10.1038/nrc2685">doi:10.1038/nrc2685</a>
</p>
<p>Author: Gemma K. Alderton</p>
<p>The CDKN2A locus encodes the tumour suppressors INK4A and ARF, which induce senescence through independent pathways. CDKN2A expression is repressed by histone H3 lysine 27 trimethylation (H3K27me3), which is mediated by polycomb group proteins. This repression is reversed in response to cellular stress, </p>
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<dc:title>Senescence: Playing games with epigenetics</dc:title>
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<dc:identifier>doi:10.1038/nrc2685</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 456 (2009)</dc:source>
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<title>Drug resistance: Getting through</title>
<link>http://dx.doi.org/10.1038/nrc2686</link>
<description>Patients with pancreatic ductal adenocarcinoma (PDA) have a poor prognosis owing to several factors that include a poor response to chemotherapy. This is strange given that pancreatic tumour cells in vitro and mice with pancreatic cancer xenografts respond to the standard chemotherapeutic gemcitabine. A </description>
<content:encoded><![CDATA[

<p>
<b>Drug resistance: Getting through</b>
</p>
<p>Nature Reviews Cancer 9, 458 (2009). <a href="http://dx.doi.org/10.1038/nrc2686">doi:10.1038/nrc2686</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>Patients with pancreatic ductal adenocarcinoma (PDA) have a poor prognosis owing to several factors that include a poor response to chemotherapy. This is strange given that pancreatic tumour cells in vitro and mice with pancreatic cancer xenografts respond to the standard chemotherapeutic gemcitabine. A </p>
]]></content:encoded>
<dc:title>Drug resistance: Getting through</dc:title>
<dc:creator>Nicola McCarthy</dc:creator>
<dc:identifier>doi:10.1038/nrc2686</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 458 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>9</prism:volume>
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<title>Angiogenesis: How Down's syndrome protects</title>
<link>http://dx.doi.org/10.1038/nrc2687</link>
<description>Sandra Ryeom, George Daley and colleagues have identified a genetic explanation for the reduced risk of developing solid tumours that is evident in individuals with Down's syndrome. Having an extra copy of Down's syndrome candidate region 1 (DSCR1), a gene on chromosome 21 </description>
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<p>
<b>Angiogenesis: How Down's syndrome protects</b>
</p>
<p>Nature Reviews Cancer 9, 456 (2009). <a href="http://dx.doi.org/10.1038/nrc2687">doi:10.1038/nrc2687</a>
</p>
<p>Author: Mhairi Skinner</p>
<p>Sandra Ryeom, George Daley and colleagues have identified a genetic explanation for the reduced risk of developing solid tumours that is evident in individuals with Down's syndrome. Having an extra copy of Down's syndrome candidate region 1 (DSCR1), a gene on chromosome 21 </p>
]]></content:encoded>
<dc:title>Angiogenesis: How Down's syndrome protects</dc:title>
<dc:creator>Mhairi Skinner</dc:creator>
<dc:identifier>doi:10.1038/nrc2687</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 456 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>9</prism:volume>
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<title>Signalling: Hedgehog doesn't...</title>
<link>http://dx.doi.org/10.1038/nrc2688</link>
<description>The role of hedgehog signalling as a driver of certain solid tumours is well established and receiving considerable translational development. Data also suggest that hedgehog signalling might be important for the development of leukaemia, potentially identifying additional patients that would benefit from anti-hedgehog therapy. However, </description>
<content:encoded><![CDATA[

<p>
<b>Signalling: Hedgehog doesn't...</b>
</p>
<p>Nature Reviews Cancer 9, 455 (2009). <a href="http://dx.doi.org/10.1038/nrc2688">doi:10.1038/nrc2688</a>
</p>
<p>Author: Gemma K. Alderton</p>
<p>The role of hedgehog signalling as a driver of certain solid tumours is well established and receiving considerable translational development. Data also suggest that hedgehog signalling might be important for the development of leukaemia, potentially identifying additional patients that would benefit from anti-hedgehog therapy. However, </p>
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<dc:title>Signalling: Hedgehog doesn't...</dc:title>
<dc:creator>Gemma K. Alderton</dc:creator>
<dc:identifier>doi:10.1038/nrc2688</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 455 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>7</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>455</prism:startingPage>
<prism:endingPage>455</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2689">
<title>Therapeutics: Dependent on KRAS</title>
<link>http://dx.doi.org/10.1038/nrc2689</link>
<description>Although activating KRAS mutations occur frequently in cancer, targeting this oncogene has proved difficult. Three groups have now identified pathways that have not been previously linked to KRAS &#8212; all of which may provide pharmacologically tractable anticancer targets &#8212; and that are crucial in </description>
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<p>
<b>Therapeutics: Dependent on KRAS</b>
</p>
<p>Nature Reviews Cancer 9, 457 (2009). <a href="http://dx.doi.org/10.1038/nrc2689">doi:10.1038/nrc2689</a>
</p>
<p>Author: Sarah Seton-Rogers</p>
<p>Although activating KRAS mutations occur frequently in cancer, targeting this oncogene has proved difficult. Three groups have now identified pathways that have not been previously linked to KRAS &#8212; all of which may provide pharmacologically tractable anticancer targets &#8212; and that are crucial in </p>
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<dc:title>Therapeutics: Dependent on KRAS</dc:title>
<dc:creator>Sarah Seton-Rogers</dc:creator>
<dc:identifier>doi:10.1038/nrc2689</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 457 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>7</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>457</prism:startingPage>
<prism:endingPage>457</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2690">
<title>In Brief</title>
<link>http://dx.doi.org/10.1038/nrc2690</link>
<description>Metastasis</description>
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<p>
<b>In Brief</b>
</p>
<p>Nature Reviews Cancer 9, 459 (2009). <a href="http://dx.doi.org/10.1038/nrc2690">doi:10.1038/nrc2690</a>
</p>
<p>Metastasis</p>
]]></content:encoded>
<dc:title>In Brief</dc:title>
<dc:identifier>doi:10.1038/nrc2690</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 459 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>7</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>459</prism:startingPage>
<prism:endingPage>459</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2691">
<title>Canine first</title>
<link>http://dx.doi.org/10.1038/nrc2691</link>
<description>The US Food and Drug administration (FDA) have approved a tyrosine kinase inhibitor, toceranib phosphate (Palladia, Pfizer Animal Health), for use in dogs to treat cutaneous mast cell tumours. Unlike other cancer treatments for pets, this drug has not previously been used in humans and </description>
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<p>
<b>Canine first</b>
</p>
<p>Nature Reviews Cancer 9, 458 (2009). <a href="http://dx.doi.org/10.1038/nrc2691">doi:10.1038/nrc2691</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>The US Food and Drug administration (FDA) have approved a tyrosine kinase inhibitor, toceranib phosphate (Palladia, Pfizer Animal Health), for use in dogs to treat cutaneous mast cell tumours. Unlike other cancer treatments for pets, this drug has not previously been used in humans and </p>
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<dc:title>Canine first</dc:title>
<dc:creator>Nicola McCarthy</dc:creator>
<dc:identifier>doi:10.1038/nrc2691</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 458 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>7</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>458</prism:startingPage>
<prism:endingPage>458</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2692">
<title>From the editors</title>
<link>http://dx.doi.org/10.1038/nrc2692</link>
<description>The old adage that 'prevention is better than cure' has not always been favoured in the cancer research community. In a Timeline article on page 508 Ann Bode and Zigang Dong cover the history of cancer prevention research, detailing the hits and misses that </description>
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<p>
<b>From the editors</b>
</p>
<p>Nature Reviews Cancer 9, 453 (2009). <a href="http://dx.doi.org/10.1038/nrc2692">doi:10.1038/nrc2692</a>
</p>
<p>The old adage that 'prevention is better than cure' has not always been favoured in the cancer research community. In a Timeline article on page 508 Ann Bode and Zigang Dong cover the history of cancer prevention research, detailing the hits and misses that </p>
]]></content:encoded>
<dc:title>From the editors</dc:title>
<dc:identifier>doi:10.1038/nrc2692</dc:identifier>
<dc:source>Nature Reviews Cancer 9, 453 (2009)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>9</prism:volume>
<prism:number>7</prism:number>
<prism:section>From The Editors</prism:section>
<prism:startingPage>453</prism:startingPage>
<prism:endingPage>453</prism:endingPage>
</item>
</rdf:RDF>
