Abstract
The aim of the present study was to evaluate the distribution of polymorphisms for the androgen receptor (AR) (CAG, StuI, GGN), SRD5A2 (Ala49Thr, Val89Leu) and CYP17 (MspA1) genes that are considered to be relevant for risk of prostate cancer. We studied 200 individuals from two cities in the State of São Paulo, by PCR, PCR-RFLP and ASOH techniques. The allelic frequencies of the autosomal markers and the StuI polymorphism of the AR gene were very similar to those described in most North American and European populations. In relation to the CAG and GGN number of repeats, the study subjects had smaller repeat lengths (mean of 20.65 and 22.38, respectively) than those described in North American, European and Chinese populations. In the present study, 30.5% of the individuals had less than 22 CAG repeats and 45.5% had less than 23 GGN repeats. When both repeat lengths are considered jointly, this Brazilian population is remarkably different from the others. Further studies on prostate cancer patients need to be conducted to assess the significance of these markers in the Brazilian population.
Highlights
In Brazil some 20,820 men will be diagnosed with prostate cancer this year alone and 7,320 men will die of the disease [1]
Polymorphisms of the androgen receptor (AR), SRD5A2 and cytochrome P450c17α (CYP17) genes were analyzed in DNA samples from 200 blood donors from the Hematology-Hemotherapy Center of the State University of Campinas (N = 118; mean age = 36.67 ± 9.76 years) and Hematology-Hemotherapy Center of the State University of São José do Rio Preto (N = 82; mean age = 39 ± 9.10 years)
When a possible association was tested, the results were negative for CAG and GGN repeats (P = 0.14) as well as for CAG repeats and StuI polymorphism (P = 0.27)
Summary
In Brazil some 20,820 men will be diagnosed with prostate cancer this year alone and 7,320 men will die of the disease [1]. Age, ethnicity and family history clearly affect the risk of prostate cancer [6]. There is evidence to support the hypothesis of hormonal etiology of prostate cancer involving androgen action [7,8]. Testosterone is synthesized from cholesterol by a series of reactions involving cytochrome P450 enzymes. DHT binds to the androgen receptor (AR), and the DHT-AR complex transactivates a number of genes with AR-responsive elements [9]. These events result in cell division in the prostate
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