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[Cancer Research 61, 4982-4984, July 1, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Polymorphisms in the Prostate Cancer Susceptibility Gene HPC2/ELAC2 in Multiplex Families and Healthy Controls1

Brian K. Suarez2, Daniela S. Gerhard, Jennifer Lin, Beth Haberer, Loan Nguyen, Niki K. Kesterson and William J. Catalona

Departments of Psychiatry [B. K. S., D. S. G., J. L.], and Genetics [B. K. S., D. S. G., L. N., N. K. K.], and Division of Urologic Surgery [B. H., W. J. C.], Washington University, School of Medicine, St. Louis, Missouri 63110

Two polymorphisms in the newly cloned prostate cancer susceptibility gene, HPC2/ELAC2, are suspected to be associated with an increased risk of developing the disease. These missense variants result in a serine (S) to leucine (L) substitution at amino acid residue 217 and an alanine (A) to threonine (T) substitution at residue 541. We genotyped these polymorphisms in 257 multiplex prostate cancer sibships and in 355 race-matched healthy unrelated controls. A significant increase in the frequency of the T allele is seen in the prostate cancer subjects compared with controls. There is, however, little evidence for excess clustering of the T allele within the multiplex families known to be segregating this allele, and there is no evidence for linkage of prostate cancer to the HPC2/ELAC2 region of chromosome 17p11.2 in these families. The T allele shows no association with either Gleason score or age-of-onset in segregating families.




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Copyright © 2001 by the American Association for Cancer Research.