18725974

Source:http://linkedlifedata.com/resource/pubmed/id/18725974

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0026882, umls-concept:C0037083, umls-concept:C0044602, umls-concept:C0069515, umls-concept:C0242957, umls-concept:C0285761, umls-concept:C0431085, umls-concept:C1150481, umls-concept:C1368105, umls-concept:C1451005, umls-concept:C1458155, umls-concept:C1521871, umls-concept:C1705325, umls-concept:C1710082
pubmed:issue	8
pubmed:dateCreated	2008-8-26
pubmed:abstractText	Dysregulated PI3K/Akt signaling occurs commonly in breast cancers and is due to HER2 amplification, PI3K mutation or PTEN inactivation. The objective of this study was to determine the role of Akt activation in breast cancer as a function of mechanism of activation and whether inhibition of Akt signaling is a feasible approach to therapy.
pubmed:grant	http://linkedlifedata.com/resource/pubmed/grant/P01CA94060
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pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/101285081
pubmed:citationSubset	IM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/Dimethyl Sulfoxide, http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt, http://linkedlifedata.com/resource/pubmed/chemical/Receptor, erbB-2
pubmed:status	MEDLINE
pubmed:issn	1932-6203
pubmed:author	pubmed-author:ChandarlapatySaratS, pubmed-author:DeFeo-JonesDeborahD, pubmed-author:HaskellKathleen MKM, pubmed-author:HuberHans EHE, pubmed-author:LeanderKaren RKR, pubmed-author:LoboJoseJ, pubmed-author:RosenNealN, pubmed-author:SheQing-BaiQB, pubmed-author:YeQingQ
pubmed:issnType	Electronic
pubmed:volume	3
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	e3065
pubmed:dateRevised	2010-11-18
pubmed:meshHeading	pubmed-meshheading:18725974-Breast Neoplasms, pubmed-meshheading:18725974-Cell Cycle, pubmed-meshheading:18725974-Dimethyl Sulfoxide, pubmed-meshheading:18725974-Female, pubmed-meshheading:18725974-G1 Phase, pubmed-meshheading:18725974-Gene Amplification, pubmed-meshheading:18725974-Humans, pubmed-meshheading:18725974-Phosphatidylinositol 3-Kinases, pubmed-meshheading:18725974-Proto-Oncogene Proteins c-akt, pubmed-meshheading:18725974-Receptor, erbB-2, pubmed-meshheading:18725974-Signal Transduction, pubmed-meshheading:18725974-Tumor Cells, Cultured
pubmed:year	2008
pubmed:articleTitle	Breast tumor cells with PI3K mutation or HER2 amplification are selectively addicted to Akt signaling.
pubmed:affiliation	Program in Molecular Pharmacology and Chemistry and Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York, United States of America.
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural