Stopping ras in its tracks

Channing J Der; Terry Van Dyke

doi:10.1016/j.cell.2007.05.031

Stopping ras in its tracks

Cell. 2007 Jun 1;129(5):855-7. doi: 10.1016/j.cell.2007.05.031.

Authors

Channing J Der¹, Terry Van Dyke

Affiliation

¹ Department of Pharmacology, University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, Chapel Hill, NC 27599, USA. cjder@med.unc.edu

PMID: 17540164
DOI: 10.1016/j.cell.2007.05.031

Abstract

Ras interacts with many downstream effectors that regulate complex cytoplasmic signaling networks. In this issue, Gupta et al. (2007) use mouse models of Ras-mediated tumorigenesis to show that the interaction of Ras with a single isoform of phosphatidylinositol 3-kinase (PI3K), called p110alpha (PIK3CA), is critical for tumor formation. This result will stimulate re-evaluation of pharmacological approaches to target Ras for cancer treatment.

Publication types

Comment

MeSH terms

Animals
Cells, Cultured
Class I Phosphatidylinositol 3-Kinases
Humans
Metabolic Networks and Pathways*
Mice
Neoplasms / drug therapy
Neoplasms / metabolism
Phosphatidylinositol 3-Kinases / genetics
Phosphatidylinositol 3-Kinases / metabolism*
Signal Transduction
ras Proteins / antagonists & inhibitors
ras Proteins / metabolism*

Substances

Phosphatidylinositol 3-Kinases
1-phosphatidylinositol 3-kinase p110 subunit, mouse
Class I Phosphatidylinositol 3-Kinases
ras Proteins