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PMID: 15876869 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Review

Mutated PI 3-kinases: cancer targets on a silver platter.

Cell cycle (Georgetown, Tex.) ·Vol. 4 ·No. 4 ·2005-04-00 ·Pages 578-81

Kang S, Bader AG, Zhao L, Vogt PK

Abstract

The PI3K signaling pathway is upregulated in numerous cancers. The catalytic subunit p110alpha of PI3K shows hot spot mutations in nearly 30% of several types of solid tumors. The most prominent of these mutations result in gain of enzymatic function, activate Akt signaling and induce oncogenic cellular transformation. The mutated p110alpha proteins are ideal targets for specific small molecule inhibitors that discriminate between the oncogenic and the wild-type forms of the enzyme. Such inhibitors could become highly effective anti-cancer drugs.

MeSH Terms
Animals Cell Cycle Gene Expression Regulation, Neoplastic Humans Models, Biological Mutation Neoplasms/genetics,metabolism Phosphatidylinositol 3-Kinases/genetics Proto-Oncogene Proteins/metabolism Signal Transduction
Chemicals
Proto-Oncogene Proteins Phosphatidylinositol 3-Kinases
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Kang Sohye
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California 92037, USA.
Bader Andreas G
Zhao Li
Vogt Peter K
Article Info
Journal
Cell cycle (Georgetown, Tex.)
Abbr.
Cell Cycle
ISSN
1551-4005
Published
2005-04-00
Epub
2005-00-07
Pages
578-81
Language
English
Region
United States
NLM ID
101137841
Subset
IM
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