1. ¹Cancer Prevention and Control Program, Department of Pharmacology and Toxicology, James Graham Brown Cancer Center, University of Louisville School of Medicine, Louisville, KY, USA
2. ²National Human Genome Center at Howard University, Washington, DC, USA
3. ³Human Cancer Genetics, Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA
4. ⁴Division of Epidemiology and Biostatistics, School of Public Health, University of Illinois at Chicago, Chicago, IL, USA
5. ⁵Department of Urology, Loyola University Stritch School of Medicine, Maywood, IL, USA
6. ⁶Brady Urological Institute, Johns Hopkins Medical Institutions, Baltimore, MD, USA
7. ⁷Divison of Urology, Howard University Hospital, Washington, DC, USA

Correspondence: Dr R Kittles, Human Cancer Genetics, Comprehensive Cancer Center, The Ohio State University, 494 Tzagournis Medical Research Facility, 420 W. 12th Avenue, Columbus, OH 43210, USA. E-mail: Kittles.2@osu.edu

Received 22 January 2006; Accepted 2 April 2006; Published online 30 May 2006.

Abstract

Apoptosis is an essential physiological process that regulates cellular proliferation. Here, we explored the effect of DNA sequence variation within the BCL-2 gene on prostate cancer susceptibility in three clinical populations, consisting of 428 African Americans, 214 Jamaicans and 218 European Americans. We observed a 70% reduced risk for prostate cancer among the European Americans who had possessed two copies of a promoter variant -938C/A. Additionally, common BCL-2 haplotypes appeared to influence prostate cancer risk; however, studies in larger data sets are needed to confirm our findings. Our data suggest that inherited BCL-2 variants may be associated with a decrease in prostate cancer susceptibility.