Secondary mutations as a mechanism of cisplatin resistance in BRCA2-mutated cancers

Wataru Sakai, Elizabeth M. Swisher, Beth Y. Karlan, Mukesh K. Agarwal, Jake Higgins, Cynthia Friedman, Emily Villegas, Céline Jacquemont, Daniel J. Farrugia, Fergus J. Couch, Nicole Urban and Toshiyasu Taniguchi ()
Additional contact information
Wataru Sakai: Division of Human Biology,
Elizabeth M. Swisher: Department of Obstetrics and Gynecology,
Beth Y. Karlan: Cedars-Sinai Medical Center, Women’s Cancer Research Institute, Los Angeles, California 90048-1865, USA
Mukesh K. Agarwal: Mayo Clinic, Rochester, Minnesota 55905, USA
Jake Higgins: University of Washington, Seattle, Washington 98195-7720, USA
Cynthia Friedman: Division of Human Biology,
Emily Villegas: Division of Human Biology,
Céline Jacquemont: Division of Human Biology,
Daniel J. Farrugia: Mayo Clinic, Rochester, Minnesota 55905, USA
Fergus J. Couch: Mayo Clinic, Rochester, Minnesota 55905, USA
Nicole Urban: Fred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024, USA
Toshiyasu Taniguchi: Division of Human Biology,

Nature, 2008, vol. 451, issue 7182, 1116-1120

Abstract: Resistance in BRCA2 cancers The platinum chemotherapeutics such as cisplatin and carboplatin are in clinical use in patients with BRCA2-mutated ovarian cancer. The initial response is generally good but most ovarian carcinomas ultimately become resistant to therapy. Two papers in this issue have identified a possible cause of this resistance as further mutation of the BRCA2 gene. Mutations in BRCA2 are associated with familial breast and ovarian cancer. Loss of BRCA2 function impairs DNA repair by homologous recombination and renders cells particular sensitive to cisplatin and also to PARP (poly (ADP-ribose) polymerase) inhibitors. The secondary 'resistance' mutations act by restoring the wild-type BRCA2 reading frame.

Date: 2008
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DOI: 10.1038/nature06633

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