No association between a tetranucleotide repeat polymorphism of CYP19 and prostate cancer.

The CYP19 gene encodes the enzyme aromatase, which plays a key role in the conversion of androgen to estrogen. The prostate is influenced by estrogen from peripheral sources as well as through aromatase activity in its stroma (1). There is evidence of elevated levels of aromatase activity and mRNA expression in stromal cells in prostate cancer as well as increasing evidence of cross-talk between estrogens and androgens in regulating gene expression in the prostate (2, 3). Moreover, estrogens compete with androgens for fastening to sex hormone binding protein, and it is believed that sex hormone binding protein synthesis is modulated by, and is a reflection of, estrogen/androgen balance (4). Thus, it is possible that genetic variations in CYP19 will alter the availability of sex steroid hormones and an individual’s risk of prostate cancer. A tetranucleotide (TTTA)n repeat polymorphism in intron 4 of the CYP19 gene is hypothesized to alter aromatase activity, and the (TTTA)7 and (TTTA)11 alleles have been associated with risk of prostate cancer in one previous study (5). The role of the CYP19 (TTTA)n repeat polymorphism in the etiology of prostate cancer thus remains unclear. We present here the results from a sibling-matched, case-control study to further clarify the potential relation of this genetic polymorphism with prostate cancer.