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Article: Beyond PTEN mutations: The PI3K pathway as an integrator of multiple inputs during tumorigenesis

TitleBeyond PTEN mutations: The PI3K pathway as an integrator of multiple inputs during tumorigenesis
Authors
Issue Date2006
Citation
Nature Reviews Cancer, 2006, v. 6, n. 3, p. 184-192 How to Cite?
AbstractThe tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K-PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies? © 2006 Nature Publishing Group.
Persistent Identifierhttp://hdl.handle.net/10722/292571
ISSN
2020 Impact Factor: 60.716
2020 SCImago Journal Rankings: 19.575
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCully, Megan-
dc.contributor.authorYou, Han-
dc.contributor.authorLevine, Arnold J.-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:56:46Z-
dc.date.available2020-11-17T14:56:46Z-
dc.date.issued2006-
dc.identifier.citationNature Reviews Cancer, 2006, v. 6, n. 3, p. 184-192-
dc.identifier.issn1474-175X-
dc.identifier.urihttp://hdl.handle.net/10722/292571-
dc.description.abstractThe tumour-suppressor phosphatase with tensin homology (PTEN) is the most important negative regulator of the cell-survival signalling pathway initiated by phosphatidylinositol 3-kinase (PI3K). Although PTEN is mutated or deleted in many tumours, deregulation of the PI3K-PTEN network also occurs through other mechanisms. Crosstalk between the PI3K pathways and other tumorigenic signalling pathways, such as those that involve Ras, p53, TOR (target of rapamycin) or DJ1, can contribute to this deregulation. How does the PI3K pathway integrate signals from numerous sources, and how can this information be used in the rational design of cancer therapies? © 2006 Nature Publishing Group.-
dc.languageeng-
dc.relation.ispartofNature Reviews Cancer-
dc.titleBeyond PTEN mutations: The PI3K pathway as an integrator of multiple inputs during tumorigenesis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1038/nrc1819-
dc.identifier.pmid16453012-
dc.identifier.scopuseid_2-s2.0-33644513730-
dc.identifier.volume6-
dc.identifier.issue3-
dc.identifier.spage184-
dc.identifier.epage192-
dc.identifier.isiWOS:000235591900013-
dc.identifier.issnl1474-175X-

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