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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">PI3K/PTEN Signaling in Angiogenesis and Tumorigenesis</title><author><name sortKey="Jiang, Bing Hua" sort="Jiang, Bing Hua" uniqKey="Jiang B" first="Bing-Hua" last="Jiang">Bing-Hua Jiang</name><affiliation><nlm:aff id="A1"> Mary Babb Randolph Cancer Center and Department of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, West Virginia 26506, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2"> Department of Pathology, Cancer Center, Nanjing Medical University, Nanjing 210029, Jiangsu, China</nlm:aff></affiliation></author><author><name sortKey="Liu, Ling Zhi" sort="Liu, Ling Zhi" uniqKey="Liu L" first="Ling-Zhi" last="Liu">Ling-Zhi Liu</name><affiliation><nlm:aff id="A1"> Mary Babb Randolph Cancer Center and Department of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, West Virginia 26506, USA</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">19595306</idno><idno type="pmc">2933405</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933405</idno><idno type="RBID">PMC:2933405</idno><idno type="doi">10.1016/S0065-230X(09)02002-8</idno><date when="2009">2009</date><idno type="wicri:Area/Pmc/Corpus">002754</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">002754</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">PI3K/PTEN Signaling in Angiogenesis and Tumorigenesis</title><author><name sortKey="Jiang, Bing Hua" sort="Jiang, Bing Hua" uniqKey="Jiang B" first="Bing-Hua" last="Jiang">Bing-Hua Jiang</name><affiliation><nlm:aff id="A1"> Mary Babb Randolph Cancer Center and Department of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, West Virginia 26506, USA</nlm:aff></affiliation><affiliation><nlm:aff id="A2"> Department of Pathology, Cancer Center, Nanjing Medical University, Nanjing 210029, Jiangsu, China</nlm:aff></affiliation></author><author><name sortKey="Liu, Ling Zhi" sort="Liu, Ling Zhi" uniqKey="Liu L" first="Ling-Zhi" last="Liu">Ling-Zhi Liu</name><affiliation><nlm:aff id="A1"> Mary Babb Randolph Cancer Center and Department of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, West Virginia 26506, USA</nlm:aff></affiliation></author></analytic><series><title level="j">Advances in cancer research</title><idno type="ISSN">0065-230X</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">Phosphatidylinositol 3-kinase (PI3K) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) signaling pathway play an important role in multiple cellular functions such as cell metabolism, proliferation, cell-cycle progression, and survival. PI3K is activated by growth factors and angiogenesis inducers such as vascular endothelial growth factor (VEGF) and angiopoietins. The amplification and mutations of PI3K and the loss of the tumor suppressor PTEN are common in various kinds of human solid tumors. The genetic alterations of upstream and downstream of PI3K signaling molecules such as receptor tyrosine kinases and AKT, respectively, are also frequently altered in human cancer. PI3K signaling regulates tumor growth and angiogenesis by activating AKT and other targets, and by inducing HIF-1 and VEGF expression. Angiogenesis is required for tumor growth and metastasis. In this review, we highlight the recent studies on the roles and mechanisms of PI3K and PTEN in regulating tumorigenesis and angiogenesis, and the roles of the downstream targets of PI3K for transmitting the signals. We also discuss the crosstalk of these signaling molecules and cellular events during tumor growth, metastasis, and tumor angiogenesis. Finally, we summarize the potential applications of PI3K, AKT, and mTOR inhibitors and their outcome in clinical trials for cancer treatment.</p></div></front></TEI><pmc article-type="research-article" xml:lang="EN"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0370416</journal-id><journal-id journal-id-type="pubmed-jr-id">262</journal-id><journal-id journal-id-type="nlm-ta">Adv Cancer Res</journal-id><journal-title>Advances in cancer research</journal-title><issn pub-type="ppub">0065-230X</issn></journal-meta><article-meta><article-id pub-id-type="pmid">19595306</article-id><article-id pub-id-type="pmc">2933405</article-id><article-id pub-id-type="doi">10.1016/S0065-230X(09)02002-8</article-id><article-id pub-id-type="manuscript">NIHMS231660</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>PI3K/PTEN Signaling in Angiogenesis and Tumorigenesis</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Jiang</surname><given-names>Bing-Hua</given-names></name><xref rid="A1" ref-type="aff">*</xref><xref rid="A2" ref-type="aff">†</xref></contrib><contrib contrib-type="author"><name><surname>Liu</surname><given-names>Ling-Zhi</given-names></name><xref rid="A1" ref-type="aff">*</xref></contrib></contrib-group><aff id="A1"><label>*</label> Mary Babb Randolph Cancer Center and Department of Microbiology, Immunology and Cell Biology, West Virginia University, Morgantown, West Virginia 26506, USA</aff><aff id="A2"><label>†</label> Department of Pathology, Cancer Center, Nanjing Medical University, Nanjing 210029, Jiangsu, China</aff><pub-date pub-type="nihms-submitted"><day>26</day><month>8</month><year>2010</year></pub-date><pub-date pub-type="ppub"><year>2009</year></pub-date><pub-date pub-type="pmc-release"><day>4</day><month>9</month><year>2010</year></pub-date><volume>102</volume><fpage>19</fpage><lpage>65</lpage><abstract><p id="P1">Phosphatidylinositol 3-kinase (PI3K) and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) signaling pathway play an important role in multiple cellular functions such as cell metabolism, proliferation, cell-cycle progression, and survival. PI3K is activated by growth factors and angiogenesis inducers such as vascular endothelial growth factor (VEGF) and angiopoietins. The amplification and mutations of PI3K and the loss of the tumor suppressor PTEN are common in various kinds of human solid tumors. The genetic alterations of upstream and downstream of PI3K signaling molecules such as receptor tyrosine kinases and AKT, respectively, are also frequently altered in human cancer. PI3K signaling regulates tumor growth and angiogenesis by activating AKT and other targets, and by inducing HIF-1 and VEGF expression. Angiogenesis is required for tumor growth and metastasis. In this review, we highlight the recent studies on the roles and mechanisms of PI3K and PTEN in regulating tumorigenesis and angiogenesis, and the roles of the downstream targets of PI3K for transmitting the signals. We also discuss the crosstalk of these signaling molecules and cellular events during tumor growth, metastasis, and tumor angiogenesis. Finally, we summarize the potential applications of PI3K, AKT, and mTOR inhibitors and their outcome in clinical trials for cancer treatment.</p></abstract><contract-num rid="ES1">R21 ES017237-03
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||CA</contract-num><contract-sponsor id="ES1">National Institute of Environmental Health Sciences : NIEHS</contract-sponsor><contract-sponsor id="HL1">National Heart, Lung, and Blood Institute : NHLBI</contract-sponsor><contract-sponsor id="CA1">National Cancer Institute : NCI</contract-sponsor></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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