title: p38 MAP kinase: a convergence point in cancer therapy.
abstract: Recent studies show that activation of p38 mitogen-activated protein kinase (MAPK) results in cancer cell apoptosis initiated by retinoids, cisplatin and other chemotherapeutic agents. The observation that divergent therapies act through a common signal transduction pathway raises the possibility of developing new anti-cancer agents that lack the side-effects caused by events upstream of p38 MAPK. Here, we review p38-MAPK-mediated tumor cell apoptosis and implications for cancer therapeutics.
authors.affiliation: Fred Hutchinson Cancer Research Center, and Department of Pediatrics, University of Washington, Seattle, WA, USA. jolson@fhcrc.org
authors.forename: James M
authors.initials: JM
authors.lastname: Olson
authors.forename: Andrew R
authors.initials: AR
authors.lastname: Hallahan
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D017209:Apoptosis; D002945:Cisplatin / Q000494:pharmacology; D015195:Drug Design; D004789:Enzyme Activation; D006801:Humans; D020935:MAP Kinase Signaling System / Q000187:drug effects; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009369:Neoplasms / Q000188:drug therapy* / Q000201:enzymology; D012176:Retinoids / Q000494:pharmacology; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D000970:Antineoplastic Agents; D012176:Retinoids; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D002945:Cisplatin