Exploiting the PI3K/AKT pathway for cancer drug discovery.
Evolving studies with several different targeted therapeutic agents are demonstrating that patients with genomic alterations of the target, including amplification, translocation and mutation, are more likely to respond to the therapy. Recent studies indicate that numerous components of the phosphatidylinositol-3-kinase (PI3K)/AKT pathway are targeted by amplification, mutation and translocation more frequently than any other pathway in cancer patients, with resultant activation of the pathway. This warrants exploiting the PI3K/AKT pathway for cancer drug discovery.
Hennessy
Bryan T
BT
Department of Molecular Therapeutics, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030, USA.
Smith
Debra L
DL
Ram
Prahlad T
PT
Lu
Yiling
Y
Mills
Gordon B
GB
D000818:Animals; D000970:Antineoplastic Agents / Q000138:chemical synthesis / Q000494:pharmacology* / Q000627:therapeutic use; D015195:Drug Design; D004341:Drug Evaluation / Q000379:methods; D005784:Gene Amplification / Q000187:drug effects; D006801:Humans; D009154:Mutation / Q000187:drug effects; D019869:Phosphatidylinositol 3-Kinases / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D051057:Proto-Oncogene Proteins c-akt / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects*; D014178:Translocation, Genetic / Q000187:drug effects
D000970:Antineoplastic Agents; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt