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<title>Getting to the stem of chronic myeloid leukaemia</title>
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<description>Tyrosine kinase inhibitor (TKI) therapy for chronic myeloid leukaemia (CML) is the consummate success story for targeted therapy, yet relapse is a nearly inevitable consequence of cessation or interruption of therapy. Primitive TKI-refractory CML stem cells are the likely source of these relapses, as they </description>
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<p>
<b>Getting to the stem of chronic myeloid leukaemia</b>
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<p>Nature Reviews Cancer 8, 341 (2008). <a href="http://dx.doi.org/10.1038/nrc2368">doi:10.1038/nrc2368</a>
</p>
<p>Authors: Michael Savona
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<p>Tyrosine kinase inhibitor (TKI) therapy for chronic myeloid leukaemia (CML) is the consummate success story for targeted therapy, yet relapse is a nearly inevitable consequence of cessation or interruption of therapy. Primitive TKI-refractory CML stem cells are the likely source of these relapses, as they </p>
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<p>
<b>Fusion of tumour cells with bone marrow-derived cells: a unifying explanation for metastasis</b>
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<p>Nature Reviews Cancer 8, 377 (2008). <a href="http://dx.doi.org/10.1038/nrc2371">doi:10.1038/nrc2371</a>
</p>
<p>Authors: John M. Pawelek
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<p>The causes of metastasis remain elusive despite vast information on cancer cells. We posit that cancer cell fusion with macrophages or other migratory bone marrow-derived cells (BMDCs) provides an explanation. BMDC&#8211;tumour hybrids have been detected in numerous animal models and recently in human cancer. Molecular </p>
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<p>
<b>The challenge of cancer control in Africa</b>
</p>
<p>Nature Reviews Cancer 8, 398 (2008). <a href="http://dx.doi.org/10.1038/nrc2372">doi:10.1038/nrc2372</a>
</p>
<p>Authors: Rebecca J. Lingwood, Peter Boyle, Alan Milburn, Twalib Ngoma, John Arbuthnott, Ruth McCaffrey, Stewart H. Kerr
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<p>While the world is focused on controlling the spread of diseases such as HIV and malaria in the developing world, another approaching epidemic has been largely overlooked. The World Heath Organization predicts that there will be 16 million new cancer cases per year in 2020 </p>
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<dc:title>The challenge of cancer control in Africa</dc:title>
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<description>This Review deals with recent progress in the immunotherapy of established (pre)malignant disease of viral or non-viral origin by synthetic vaccines capable of inducing robust T-cell responses. The most attractive vaccine compounds are synthetic long peptides (SLP) corresponding to the sequence of tumour viral antigens </description>
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<p>
<b>Immunotherapy of established (pre)malignant disease by synthetic long peptide vaccines</b>
</p>
<p>Nature Reviews Cancer 8, 351 (2008). <a href="http://dx.doi.org/10.1038/nrc2373">doi:10.1038/nrc2373</a>
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<p>Authors: Cornelis J.M. Melief
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<p>This Review deals with recent progress in the immunotherapy of established (pre)malignant disease of viral or non-viral origin by synthetic vaccines capable of inducing robust T-cell responses. The most attractive vaccine compounds are synthetic long peptides (SLP) corresponding to the sequence of tumour viral antigens </p>
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<description>Increases in cytosolic free Ca2+ ([Ca2+]i) represent a ubiquitous signalling mechanism that controls a variety of cellular processes, including proliferation, metabolism and gene transcription, yet under certain conditions increases in intracellular Ca2+ are cytotoxic. Thus, in using </description>
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<p>
<b>Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival</b>
</p>
<p>Nature Reviews Cancer 8, 361 (2008). <a href="http://dx.doi.org/10.1038/nrc2374">doi:10.1038/nrc2374</a>
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<p>Authors: H. Llewelyn Roderick
&amp; Simon J. Cook</p>
<p>Increases in cytosolic free Ca2+ ([Ca2+]i) represent a ubiquitous signalling mechanism that controls a variety of cellular processes, including proliferation, metabolism and gene transcription, yet under certain conditions increases in intracellular Ca2+ are cytotoxic. Thus, in using </p>
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<description>Most cancer deaths are caused by haematogenous metastatic spread and subsequent growth of tumour cells at distant organs. Disseminating tumour cells present in the peripheral blood and bone marrow can now be detected and characterized at the single-cell level. These cells are highly relevant to </description>
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<p>
<b>Detection, clinical relevance and specific biological properties of disseminating tumour cells</b>
</p>
<p>Nature Reviews Cancer 8, 329 (2008). <a href="http://dx.doi.org/10.1038/nrc2375">doi:10.1038/nrc2375</a>
</p>
<p>Authors: Klaus Pantel, Ruud H. Brakenhoff
&amp; Burkhard Brandt</p>
<p>Most cancer deaths are caused by haematogenous metastatic spread and subsequent growth of tumour cells at distant organs. Disseminating tumour cells present in the peripheral blood and bone marrow can now be detected and characterized at the single-cell level. These cells are highly relevant to </p>
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<dc:title>Detection, clinical relevance and specific biological properties of disseminating tumour cells</dc:title>
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<dc:creator>Burkhard Brandt</dc:creator>
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<dc:source>Nature Reviews Cancer 8, 329 (2008)</dc:source>
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<title>Therapy: Bad to the bone</title>
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<description>Evidence that suppressing the hedgehog (Hh) signalling pathway in cancers has potential therapeutic value has led to the development of drugs that target this pathway. However, results from Tom Curran and colleagues indicate that suppressing Hh signalling in young mice results in permanent and detrimental </description>
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<p>
<b>Therapy: Bad to the bone</b>
</p>
<p>Nature Reviews Cancer 8, 323 (2008). <a href="http://dx.doi.org/10.1038/nrc2376">doi:10.1038/nrc2376</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>Evidence that suppressing the hedgehog (Hh) signalling pathway in cancers has potential therapeutic value has led to the development of drugs that target this pathway. However, results from Tom Curran and colleagues indicate that suppressing Hh signalling in young mice results in permanent and detrimental </p>
]]></content:encoded>
<dc:title>Therapy: Bad to the bone</dc:title>
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<dc:identifier>doi:10.1038/nrc2376</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 323 (2008)</dc:source>
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<title>Tumour suppressors: Motoring on down</title>
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<description>Deletion of the outermost band of the short arm of chromosome 1 (1p36) is often seen in multiple tumour types, including neural crest-derived tumours, giving rise to the hypothesis that this region harbours one or more tumour suppressor genes. Susan Schlisio, Bill Kaelin and colleagues </description>
<content:encoded><![CDATA[

<p>
<b>Tumour suppressors: Motoring on down</b>
</p>
<p>Nature Reviews Cancer 8, 326 (2008). <a href="http://dx.doi.org/10.1038/nrc2377">doi:10.1038/nrc2377</a>
</p>
<p>Author: Nicola McCarthy</p>
<p>Deletion of the outermost band of the short arm of chromosome 1 (1p36) is often seen in multiple tumour types, including neural crest-derived tumours, giving rise to the hypothesis that this region harbours one or more tumour suppressor genes. Susan Schlisio, Bill Kaelin and colleagues </p>
]]></content:encoded>
<dc:title>Tumour suppressors: Motoring on down</dc:title>
<dc:creator>Nicola McCarthy</dc:creator>
<dc:identifier>doi:10.1038/nrc2377</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 326 (2008)</dc:source>
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<title>Signalling: An oncogene becomes RESTless</title>
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<description>REST (repressor-element-1 silencing transcription factor) is a transcriptional repressor that is associated with the maintainenance of neuron stem cell self-renewal and has been characterized as an oncogene in neuronal stem cells and, paradoxically, as a tumour suppressor in epithelial tissues. How REST accomplishes these </description>
<content:encoded><![CDATA[

<p>
<b>Signalling: An oncogene becomes RESTless</b>
</p>
<p>Nature Reviews Cancer 8, 327 (2008). <a href="http://dx.doi.org/10.1038/nrc2378">doi:10.1038/nrc2378</a>
</p>
<p>Author: Gemma K. Alderton</p>
<p>REST (repressor-element-1 silencing transcription factor) is a transcriptional repressor that is associated with the maintainenance of neuron stem cell self-renewal and has been characterized as an oncogene in neuronal stem cells and, paradoxically, as a tumour suppressor in epithelial tissues. How REST accomplishes these </p>
]]></content:encoded>
<dc:title>Signalling: An oncogene becomes RESTless</dc:title>
<dc:creator>Gemma K. Alderton</dc:creator>
<dc:identifier>doi:10.1038/nrc2378</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 327 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
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<title>Tumorigenesis: Ready and waiting</title>
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<description>How does the oncogenic transcription factor MYC promote cell proliferation? Although MYC binds to at least 11% of promoters in the human genome and this binding contributes to (but is not always sufficient for) gene expression to promote cell growth, the mechanism and key </description>
<content:encoded><![CDATA[

<p>
<b>Tumorigenesis: Ready and waiting</b>
</p>
<p>Nature Reviews Cancer 8, 322 (2008). <a href="http://dx.doi.org/10.1038/nrc2379">doi:10.1038/nrc2379</a>
</p>
<p>Author: Gemma K. Alderton</p>
<p>How does the oncogenic transcription factor MYC promote cell proliferation? Although MYC binds to at least 11% of promoters in the human genome and this binding contributes to (but is not always sufficient for) gene expression to promote cell growth, the mechanism and key </p>
]]></content:encoded>
<dc:title>Tumorigenesis: Ready and waiting</dc:title>
<dc:creator>Gemma K. Alderton</dc:creator>
<dc:identifier>doi:10.1038/nrc2379</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 322 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
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<title>Metastasis: Bringing up the rear</title>
<link>http://dx.doi.org/10.1038/nrc2380</link>
<description>The extent of the requirement for functional migration machinery in tumour dissemination remains unclear. In Cancer Cell, James Quigley and colleagues report that blocking the function of the tetraspanin CD151in vivo prevents tumour dissemination by inhibiting migration and access to the vasculature </description>
<content:encoded><![CDATA[

<p>
<b>Metastasis: Bringing up the rear</b>
</p>
<p>Nature Reviews Cancer 8, 326 (2008). <a href="http://dx.doi.org/10.1038/nrc2380">doi:10.1038/nrc2380</a>
</p>
<p>Author: Kim Baumann</p>
<p>The extent of the requirement for functional migration machinery in tumour dissemination remains unclear. In Cancer Cell, James Quigley and colleagues report that blocking the function of the tetraspanin CD151in vivo prevents tumour dissemination by inhibiting migration and access to the vasculature </p>
]]></content:encoded>
<dc:title>Metastasis: Bringing up the rear</dc:title>
<dc:creator>Kim Baumann</dc:creator>
<dc:identifier>doi:10.1038/nrc2380</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 326 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
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<title>Signalling: Stress and disease connect at mTORC1</title>
<link>http://dx.doi.org/10.1038/nrc2381</link>
<description>Loss of the tuberous sclerosis complex (TSC) genes TSC1 and TSC2 leads to constitutive activation of the mammalian target of rapamycin complex-1 (mTORC1) and downstream signalling components, resulting in insulin resistance, the development of tumours and neurological disorders. Hotamisligil and colleagues now reveal </description>
<content:encoded><![CDATA[

<p>
<b>Signalling: Stress and disease connect at mTORC1</b>
</p>
<p>Nature Reviews Cancer 8, 325 (2008). <a href="http://dx.doi.org/10.1038/nrc2381">doi:10.1038/nrc2381</a>
</p>
<p>Author: Ekat Kritikou</p>
<p>Loss of the tuberous sclerosis complex (TSC) genes TSC1 and TSC2 leads to constitutive activation of the mammalian target of rapamycin complex-1 (mTORC1) and downstream signalling components, resulting in insulin resistance, the development of tumours and neurological disorders. Hotamisligil and colleagues now reveal </p>
]]></content:encoded>
<dc:title>Signalling: Stress and disease connect at mTORC1</dc:title>
<dc:creator>Ekat Kritikou</dc:creator>
<dc:identifier>doi:10.1038/nrc2381</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 325 (2008)</dc:source>
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<title>Signalling: Follow your eNOS</title>
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<description>The Achilles heel of many tumours is thought to be their 'addiction' to or dependence on specific factors and pathways, such as activation of the phosphatidylinositol 3-kinase (PI3K)&#8722;Akt signalling pathway in tumour cells expressing oncogenic Ras. But what is it about these factors that tumours </description>
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<p>
<b>Signalling: Follow your eNOS</b>
</p>
<p>Nature Reviews Cancer 8, 322 (2008). <a href="http://dx.doi.org/10.1038/nrc2382">doi:10.1038/nrc2382</a>
</p>
<p>Author: Kristine Novak</p>
<p>The Achilles heel of many tumours is thought to be their 'addiction' to or dependence on specific factors and pathways, such as activation of the phosphatidylinositol 3-kinase (PI3K)&#8722;Akt signalling pathway in tumour cells expressing oncogenic Ras. But what is it about these factors that tumours </p>
]]></content:encoded>
<dc:title>Signalling: Follow your eNOS</dc:title>
<dc:creator>Kristine Novak</dc:creator>
<dc:identifier>doi:10.1038/nrc2382</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 322 (2008)</dc:source>
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<title>Carcinogenesis: Predisposing to behaviour?</title>
<link>http://dx.doi.org/10.1038/nrc2383</link>
<description>Tobacco is well-established as a carcinogen associated with lung cancer. However, epidemiological studies also suggest that a familial risk of developing lung cancer exists, pointing toward genetic predisposition in the aetiology of the disease. Three genome-wide association studies (GWASs) indicate that genetic variation might </description>
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<p>
<b>Carcinogenesis: Predisposing to behaviour?</b>
</p>
<p>Nature Reviews Cancer 8, 321 (2008). <a href="http://dx.doi.org/10.1038/nrc2383">doi:10.1038/nrc2383</a>
</p>
<p>Author: Gemma K. Alderton</p>
<p>Tobacco is well-established as a carcinogen associated with lung cancer. However, epidemiological studies also suggest that a familial risk of developing lung cancer exists, pointing toward genetic predisposition in the aetiology of the disease. Three genome-wide association studies (GWASs) indicate that genetic variation might </p>
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<dc:title>Carcinogenesis: Predisposing to behaviour?</dc:title>
<dc:creator>Gemma K. Alderton</dc:creator>
<dc:identifier>doi:10.1038/nrc2383</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 321 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>321</prism:startingPage>
<prism:endingPage>321</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2384">
<title>Tumour microenvironment: No changes necessary</title>
<link>http://dx.doi.org/10.1038/nrc2384</link>
<description>Does the key role of the tumour microenvironment in driving tumorigenesis depend on somatic genetic alterations in the stromal cells? The evidence has been divided, but new research using high-resolution single nucleotide polymorphism (SNP) array technology shows that carcinoma-associated fibroblasts (CAFs) display little evidence of </description>
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<p>
<b>Tumour microenvironment: No changes necessary</b>
</p>
<p>Nature Reviews Cancer 8, 324 (2008). <a href="http://dx.doi.org/10.1038/nrc2384">doi:10.1038/nrc2384</a>
</p>
<p>Author: Patrick Goymer</p>
<p>Does the key role of the tumour microenvironment in driving tumorigenesis depend on somatic genetic alterations in the stromal cells? The evidence has been divided, but new research using high-resolution single nucleotide polymorphism (SNP) array technology shows that carcinoma-associated fibroblasts (CAFs) display little evidence of </p>
]]></content:encoded>
<dc:title>Tumour microenvironment: No changes necessary</dc:title>
<dc:creator>Patrick Goymer</dc:creator>
<dc:identifier>doi:10.1038/nrc2384</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>324</prism:startingPage>
<prism:endingPage>325</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2385">
<title>Oncogenes: Sibling rivalry explained</title>
<link>http://dx.doi.org/10.1038/nrc2385</link>
<description>The proteins encoded by the oncogenes KRAS and NRAS are highly homologous and have similar enzymatic functions, but mutations in KRAS are found in nearly 50% of human colon cancers, whereas only about 5% occur in NRAS. In their Nature Genetics</description>
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<p>
<b>Oncogenes: Sibling rivalry explained</b>
</p>
<p>Nature Reviews Cancer 8, 324 (2008). <a href="http://dx.doi.org/10.1038/nrc2385">doi:10.1038/nrc2385</a>
</p>
<p>Author: Isobel Barry</p>
<p>The proteins encoded by the oncogenes KRAS and NRAS are highly homologous and have similar enzymatic functions, but mutations in KRAS are found in nearly 50% of human colon cancers, whereas only about 5% occur in NRAS. In their Nature Genetics</p>
]]></content:encoded>
<dc:title>Oncogenes: Sibling rivalry explained</dc:title>
<dc:creator>Isobel Barry</dc:creator>
<dc:identifier>doi:10.1038/nrc2385</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>324</prism:startingPage>
<prism:endingPage>325</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2386">
<title>The devil with the details</title>
<link>http://dx.doi.org/10.1038/nrc2386</link>
<description>The outlook was bleak for the Tasmanian devil until Cedric came along. Numbers have been devastated in the past 12 years by the mysterious devil facial tumour disease, which causes tumorous growths on an affected animal's face and neck that eventually make it unable to </description>
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<p>
<b>The devil with the details</b>
</p>
<p>Nature Reviews Cancer 8, 324 (2008). <a href="http://dx.doi.org/10.1038/nrc2386">doi:10.1038/nrc2386</a>
</p>
<p>Author: Isobel Barry</p>
<p>The outlook was bleak for the Tasmanian devil until Cedric came along. Numbers have been devastated in the past 12 years by the mysterious devil facial tumour disease, which causes tumorous growths on an affected animal's face and neck that eventually make it unable to </p>
]]></content:encoded>
<dc:title>The devil with the details</dc:title>
<dc:creator>Isobel Barry</dc:creator>
<dc:identifier>doi:10.1038/nrc2386</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 324 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>324</prism:startingPage>
<prism:endingPage>324</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2387">
<title>Don't stop now!</title>
<link>http://dx.doi.org/10.1038/nrc2387</link>
<description>A recent study published in the Annals of Oncology indicates a worrying trend for terminating clinical trials for efficacious new cancer drugs early, raising the possibility that important safety data might be missed.The study examined randomized controlled trials (RCTs) published between 1997 and </description>
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<p>
<b>Don't stop now!</b>
</p>
<p>Nature Reviews Cancer 8, 322 (2008). <a href="http://dx.doi.org/10.1038/nrc2387">doi:10.1038/nrc2387</a>
</p>
<p>A recent study published in the Annals of Oncology indicates a worrying trend for terminating clinical trials for efficacious new cancer drugs early, raising the possibility that important safety data might be missed.The study examined randomized controlled trials (RCTs) published between 1997 and </p>
]]></content:encoded>
<dc:title>Don't stop now!</dc:title>
<dc:identifier>doi:10.1038/nrc2387</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 322 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Research Highlight</prism:section>
<prism:startingPage>322</prism:startingPage>
<prism:endingPage>322</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2388">
<title>From the editors</title>
<link>http://dx.doi.org/10.1038/nrc2388</link>
<description>What are the most important factors that should be considered when treating cancer? Many would argue that the process of metastasis is one, given that metastases are the cause of death for most cancer patients. The metastatic process is complex and it appears that the </description>
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<p>
<b>From the editors</b>
</p>
<p>Nature Reviews Cancer 8, 319 (2008). <a href="http://dx.doi.org/10.1038/nrc2388">doi:10.1038/nrc2388</a>
</p>
<p>What are the most important factors that should be considered when treating cancer? Many would argue that the process of metastasis is one, given that metastases are the cause of death for most cancer patients. The metastatic process is complex and it appears that the </p>
]]></content:encoded>
<dc:title>From the editors</dc:title>
<dc:identifier>doi:10.1038/nrc2388</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 319 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>From The Editors</prism:section>
<prism:startingPage>319</prism:startingPage>
<prism:endingPage>319</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2389">
<title>Wnt signalling and its impact on development and cancer</title>
<link>http://dx.doi.org/10.1038/nrc2389</link>
<description>The Wnt signalling pathway is an ancient system that has been highly conserved during evolution. It has a crucial role in the embryonic development of all animal species, in the regeneration of tissues in adult organisms and in many other processes. Mutations or deregulated expression </description>
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<p>
<b>Wnt signalling and its impact on development and cancer</b>
</p>
<p>Nature Reviews Cancer 8, 387 (2008). <a href="http://dx.doi.org/10.1038/nrc2389">doi:10.1038/nrc2389</a>
</p>
<p>Authors: Alexandra Klaus
&amp; Walter Birchmeier</p>
<p>The Wnt signalling pathway is an ancient system that has been highly conserved during evolution. It has a crucial role in the embryonic development of all animal species, in the regeneration of tissues in adult organisms and in many other processes. Mutations or deregulated expression </p>
]]></content:encoded>
<dc:title>Wnt signalling and its impact on development and cancer</dc:title>
<dc:creator>Alexandra Klaus</dc:creator>
<dc:creator>Walter Birchmeier</dc:creator>
<dc:identifier>doi:10.1038/nrc2389</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 387 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Perspective</prism:section>
<prism:startingPage>387</prism:startingPage>
<prism:endingPage>398</prism:endingPage>
</item>
<item rdf:about="http://dx.doi.org/10.1038/nrc2395">
<title>Prostate-specific antigen and prostate cancer: prediction, detection and monitoring (Corrigendum)</title>
<link>http://dx.doi.org/10.1038/nrc2395</link>
<description>Nature Reviews Cancer8, 268&#8211;278 (2008)There is an error in the legend of FIG. 4 on page 275 of this article. The hk2 level in seminal fluid is given incorrectly; it should read 2&#8211;12 &#956;g/ml.</description>
<content:encoded><![CDATA[

<p>
<b>Prostate-specific antigen and prostate cancer: prediction, detection and monitoring (Corrigendum)</b>
</p>
<p>Nature Reviews Cancer 8, 404 (2008). <a href="http://dx.doi.org/10.1038/nrc2395">doi:10.1038/nrc2395</a>
</p>
<p>Author: Hans Lilja, David Ulmert
&amp; Andrew J. Vickers</p>
<p>Nature Reviews Cancer8, 268&#8211;278 (2008)There is an error in the legend of FIG. 4 on page 275 of this article. The hk2 level in seminal fluid is given incorrectly; it should read 2&#8211;12 &#956;g/ml.</p>
]]></content:encoded>
<dc:title>Prostate-specific antigen and prostate cancer: prediction, detection and monitoring (Corrigendum)</dc:title>
<dc:creator>Hans Lilja</dc:creator>
<dc:creator>David Ulmert</dc:creator>
<dc:creator>Andrew J. Vickers</dc:creator>
<dc:identifier>doi:10.1038/nrc2395</dc:identifier>
<dc:source>Nature Reviews Cancer 8, 404 (2008)</dc:source>
<prism:publicationName>Nature Reviews Cancer</prism:publicationName>
<prism:volume>8</prism:volume>
<prism:number>5</prism:number>
<prism:section>Corrigendum</prism:section>
<prism:startingPage>404</prism:startingPage>
<prism:endingPage>404</prism:endingPage>
</item>
</rdf:RDF>
