1. ¹Division of Surgery and Oncology, School of Cancer Studies, University of Liverpool, Liverpool, UK
2. ²The Breakthrough Toby Robins Breast Cancer Research Centre, Chester Beatty Laboratories, The Institute of Cancer Research, London, UK
3. ³EORTC Data Center, Brussels, Belgium
4. ⁴Clatterbridge Centre for Oncology NHS Trust, Wirral Merseyside, UK
5. ⁵Erasmus University Medical Center, Rotterdam, The Netherlands
6. ⁶Lung and Mesothelioma Unit, Department of Medical Oncology, St Bartholomew's Hospital, London, UK

Correspondence: Dr JA Green, Division of Surgery and Oncology, School of Cancer Studies, University of Liverpool, Liverpool L7 8XP, UK. E-mail: J.A.Green@liverpool.ac.uk

Received 13 August 2007; Revised 26 February 2008; Accepted 3 March 2008.

Abstract

The Fanconi gene family has a role in DNA repair and inactivation of FANCF has been proposed as a mechanism of sensitisation to platinum chemotherapy. This study sought to confirm this hypothesis in cell lines and a large series of ovarian cancer samples. Promoter methylation was assessed by methylation-sensitive polymerase chain reaction of FANCF in nine ovarian cancer cell lines and 74 ovarian cancer samples taken from patients entered on a trial of cisplatin-based chemotherapy. This study confirmed methylation-dependent silencing of FANCF in one out of nine ovarian cancer cell lines. Methylation of FANCF was demonstrated in 13.2% of 53 evaluable ovarian tumour samples. Progression-free survival gave an HR of 3.63 (95% CI: 1.54–8.54, P=0.0016) in favour of the unmethylated cases. There was no association with overall survival. This study does not support methylation-dependent silencing of FANCF as a mechanism of sensitisation to platinum-based chemotherapy in ovarian cancer.