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Open AccessResearch article

No major association between TGFBR1*6A and prostate cancer

Virginia Kaklamani1 email, Lisa Baddi1 email, Diana Rosman1 email, Junjian Liu1 email, Nathan Ellis2 email, Carole Oddoux3 email, Harry Ostrer3 email, Yu Chen4 email, Habibul Ahsan4 email, Kenneth Offit2 email and Boris Pasche1 email

Cancer Genetics Program, Division of Hematology/Oncology, Department of Medicine and Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA

Clinical Genetics Service, Memorial Sloan-Kettering Cancer Center, New York, New York, USA

Human Genetics Program, Department of Pediatrics, New York University Medical Center, New York, N.Y., 10016, USA

Department of Epidemiology of Mailman School of Public Health and Herbert Irving Comprehensive Cancer Center, Columbia University, New York, New York, USA

author email corresponding author email

BMC Genetics 2004, 5:28doi:10.1186/1471-2156-5-28

Published: 22 September 2004

Abstract

Prostate cancer is the most commonly diagnosed cancer in men and one of the leading causes of cancer deaths. There is strong genetic evidence indicating that a large proportion of prostate cancers are caused by heritable factors but the search for prostate cancer susceptibility genes has thus far remained elusive. TGFBR1*6A, a common hypomorphic variant of the type I Transforming Growth Factor Beta receptor, is emerging as a tumor susceptibility allele that predisposes to the development of breast, colon and ovarian cancer. The association with prostate cancer has not yet been explored. A total of 907 cases and controls from New York City were genotyped to test the hypothesis that TGFBR1*6A may contribute to the development of prostate cancer. TGFBR1*6A allelic frequency among cases (0.086) was slightly higher than among controls (0.080) but the differences in TGFBR1*6A genotype distribution between cases and controls did not reach statistical significance (p = 0.67). Our data suggest that TGFBR1*6A does not contribute to the development of prostate cancer.


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