Resistance to therapy caused by intragenic deletion in BRCA2

Stacey L. Edwards, Rachel Brough, Christopher J. Lord, Rachael Natrajan, Radost Vatcheva, Douglas A. Levine, Jeff Boyd, Jorge S. Reis-Filho and Alan Ashworth ()
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Stacey L. Edwards: The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK
Rachel Brough: The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK
Christopher J. Lord: The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK
Rachael Natrajan: The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK
Radost Vatcheva: The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK
Douglas A. Levine: Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
Jeff Boyd: Anderson Cancer Institute, Memorial Health University Medical Center, 4700 Waters Avenue, Savannah, GA 31404, USA
Jorge S. Reis-Filho: The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK
Alan Ashworth: The Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, Fulham Road, London SW3 6JB, UK

Nature, 2008, vol. 451, issue 7182, 1111-1115

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/nature06548

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