Drug-resistant phosphatidylinositol 3-kinase: guidance for the preemptive strike.
In this issue of Cancer Cell, Zunder et al. (2008) describe surprising findings from investigating inhibitor-resistant mutations in the affinity pocket of p110 alpha of phosphatidylinositol 3-kinase (PI3K). Information on these critical residues provides a road map for generating novel PI3K inhibitors that can overcome the anticipated resistance mutations.
Vogt
Peter K
PK
Division of Oncovirology, The Scripps Research Institute, La Jolla, CA 92037, USA. pkvogt@scripps.edu
D000818:Animals; D058534:Class I Phosphatidylinositol 3-Kinases; D019008:Drug Resistance, Neoplasm / Q000187:drug effects; D006801:Humans; D007527:Isoenzymes / Q000378:metabolism; D051379:Mice; D009154:Mutation / Q000235:genetics; D015513:Oncogene Proteins / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D012441:Saccharomyces cerevisiae / Q000254:growth & development
D058534:Class I Phosphatidylinositol 3-Kinases; D007527:Isoenzymes; D015513:Oncogene Proteins; D019869:Phosphatidylinositol 3-Kinases; D047428:Protein Kinase Inhibitors; C484760:PIK3CA protein, human