p38 MAP kinase: a convergence point in cancer therapy

James M Olson; Andrew R Hallahan

doi:10.1016/j.molmed.2004.01.007

p38 MAP kinase: a convergence point in cancer therapy

Trends Mol Med. 2004 Mar;10(3):125-9. doi: 10.1016/j.molmed.2004.01.007.

Authors

James M Olson¹, Andrew R Hallahan

Affiliation

¹ Fred Hutchinson Cancer Research Center, and Department of Pediatrics, University of Washington, Seattle, WA, USA. jolson@fhcrc.org

PMID: 15102355
DOI: 10.1016/j.molmed.2004.01.007

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.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Antineoplastic Agents / pharmacology
Antineoplastic Agents / therapeutic use
Apoptosis
Cisplatin / pharmacology
Drug Design
Enzyme Activation
Humans
MAP Kinase Signaling System / drug effects
Mitogen-Activated Protein Kinases / antagonists & inhibitors*
Mitogen-Activated Protein Kinases / metabolism
Neoplasms / drug therapy*
Neoplasms / enzymology
Retinoids / pharmacology
p38 Mitogen-Activated Protein Kinases

Substances

Antineoplastic Agents
Retinoids
Mitogen-Activated Protein Kinases
p38 Mitogen-Activated Protein Kinases
Cisplatin