Research Article

Genetic polymorphism in sex hormone metabolism and prostate cancer risk

Published: July 03, 2015
Genet. Mol. Res. 14 (3) : 7326-7334 DOI: 10.4238/2015.July.3.8

Abstract

We compared single-nucleotide polymorphisms for point mutations in cytochrome P450 genes, including cytochrome P450c17α (CYP17), cytochrome P450 aromatase (CYP19), steroid-5-a-reductase (SRD5A2), and prostate-specific antigen (PSA) involved in androgen and estrogen production. Between January 2008 and January 2010, 90 patients were enrolled in the study. Of these patients, 28 were diagnosed with benign prostatic hyperplasia and 32 with prostate cancer, while 30 subjects were included as a control group. CYP19 1531 C>T, SRD5A2 gene V89L, CYP17 gene -34 T/C, PSA-158 (G/A) regions were evalu­ated for the association between polymorphisms and benign prostatic hyperplasia and prostate cancer in study population. Age, body mass index, peak urinary flow rate (Q max), voided urine volume, post-void residual urine volume, total PSA, free PSA, free/total PSA ratio, pros­tate weights measured by transrectal ultrasonography, erectile dysfunc­tion score, and international prostate symptom score were compared between groups. No statistically significant difference in CYP19 1531 C>T, SRD5A2 V89L, and CYP17 -34T/C was observed in both groups when compared to the control group. The homozygote variant of PSA- 158 (G/A) was significantly lower for prostate cancer. Age, total PSA, free PSA, free/total PSA ratio, prostate weight, and Q max were evalu­ated using multi-variant analysis. Only Q max was significant for the homozygote variant. The probability of being homozygous was 5.8- fold higher in subjects with Q max >14 mL/s. In the Turkish population, the homozygote variant of PSA-158 (G/A) was significantly lower for prostate cancer.

We compared single-nucleotide polymorphisms for point mutations in cytochrome P450 genes, including cytochrome P450c17α (CYP17), cytochrome P450 aromatase (CYP19), steroid-5-a-reductase (SRD5A2), and prostate-specific antigen (PSA) involved in androgen and estrogen production. Between January 2008 and January 2010, 90 patients were enrolled in the study. Of these patients, 28 were diagnosed with benign prostatic hyperplasia and 32 with prostate cancer, while 30 subjects were included as a control group. CYP19 1531 C>T, SRD5A2 gene V89L, CYP17 gene -34 T/C, PSA-158 (G/A) regions were evalu­ated for the association between polymorphisms and benign prostatic hyperplasia and prostate cancer in study population. Age, body mass index, peak urinary flow rate (Q max), voided urine volume, post-void residual urine volume, total PSA, free PSA, free/total PSA ratio, pros­tate weights measured by transrectal ultrasonography, erectile dysfunc­tion score, and international prostate symptom score were compared between groups. No statistically significant difference in CYP19 1531 C>T, SRD5A2 V89L, and CYP17 -34T/C was observed in both groups when compared to the control group. The homozygote variant of PSA- 158 (G/A) was significantly lower for prostate cancer. Age, total PSA, free PSA, free/total PSA ratio, prostate weight, and Q max were evalu­ated using multi-variant analysis. Only Q max was significant for the homozygote variant. The probability of being homozygous was 5.8- fold higher in subjects with Q max >14 mL/s. In the Turkish population, the homozygote variant of PSA-158 (G/A) was significantly lower for prostate cancer.