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The Common D302H Variant of CASP8 Is Associated with Risk of Glioma

¹ Section of Cancer Genetics and ² Section of Epidemiology, Institute of Cancer Research, Sutton, Surrey, United Kingdom; ³ Department of Epidemiology, Tampere School of Public Health, University of Tampere, Tampere, Finland; ⁴ Department of Research and Environmental Surveillance, Radiation and Nuclear Safety Authority, Radiation and Nuclear Safety Authority, Helsinki, Finland; ⁵ Institute of Cancer Epidemiology, Danish Cancer Society, Copenhagen, Denmark; ⁶ Division of Epidemiology and Public Health, University of Nottingham Medical School, Queen's Medical Centre, Nottingham, United Kingdom; ⁷ Centre for Epidemiology and Biostatistics, Leeds, United Kingdom; ⁸ Division of Epidemiology, Institute of Environmental Medicine and ⁹ Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; and ¹⁰ Department of Radiation Sciences, Umeå University, Umeå, Sweden

Requests for reprints: Richard Houlston, Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK. Phone: 44-0-208-722-4175; Fax: 44-0-208-722-4359. E-mail: richard.houlston{at}icr.ac.uk

Caspase 8 (CASP8) is a key regulator of apoptosis or programmed cell death, and, hence, a defense against cancer. We tested the hypothesis that the CASP8 polymorphism D302H influences risk of glioma through analysis of five series of glioma case patients and controls (n = 1,005 and 1,011, respectively). Carrier status for the rare allele of D302H was associated with a 1.37-fold increased risk (95% confidence interval, 1.10-1.70; P = 0.004). The association of CASP8 D302H with glioma risk indicates the importance of inherited variation in the apoptosis pathway in susceptibility to this form of primary brain tumor. (Cancer Epidemiol Biomarkers Prev 2008;17(4):987–9)