title: Stopping ras in its tracks.
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.
authors.affiliation: Department of Pharmacology, University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, Chapel Hill, NC 27599, USA. cjder@med.unc.edu
authors.forename: Channing J
authors.initials: CJ
authors.lastname: Der
authors.forename: Terry
authors.initials: T
authors.lastname: Van Dyke
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D058534:Class I Phosphatidylinositol 3-Kinases; D006801:Humans; D053858:Metabolic Networks and Pathways; D051379:Mice; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D018631:ras Proteins / Q000037:antagonists & inhibitors / Q000378:metabolism*
chemical_list: D019869:Phosphatidylinositol 3-Kinases; C509622:1-phosphatidylinositol 3-kinase p110 subunit, mouse; D058534:Class I Phosphatidylinositol 3-Kinases; D018631:ras Proteins