Balkan Journal of Medical Genetics

POLYMORPHISMS OF HPC2/ELAC2 AND SRD5A2 (5α-Reductase Type II) GENES IN PROSTATE CANCER
İzmirli M1,*, Arikan B2, Bayazit Y3, Alptekin D4
*Corresponding Author: Muzeyyen İzmirli, Department of Medical Biology, Faculty of Medicine, Bezmialem Vakif University, 34093, Istanbul, Turkey; Tel.: +90-212-523-37-19, Fax: +90-212-523-23-26; E-mail: muzeyyenizmirli@gmail.com.
page: 31

RESULTS

The allele frequencies of Ser217Leu and Ala541Thr polymorphisms at the HPC2/ELAC2 gene in the cancer and the control subjects were in Hardy-Weinberg equilibrium. The allele frequencies of Ser217 and Leu217 in the cancer patients were 52.3 and 47.7%, respectively, and for the control groups were 82.4 and 17.6%, respectively (Table 1). The difference between the patients and controls for the Ser217Leu polymorphism was significant. This shows that there was a noteworthy relation at risk of prostate cancer between cases and controls for the HPC2/ELAC2 gene Ser217- Leu polymorphism [odds ratio (OR) 2.7; confidence interval 95% (CI 95%) 1.6-4.8; p 0.000<0.05]. Allele frequencies for Ala541 and Thr541 in the patients were 95.3 and 4.7%, respectively, and 97.1 and 2.9% respectively, for the controls (Table 2). There was no difference between the patient and control groups regarding the Ala541Thr polymorphism (OR 1.4; CI 95% 0.4-0.7; p 0.556, p >0.05). The genotype frequencies for the Ala49Thr and Val89 Leu polymorphisms in the SRD5A2 gene were in Hardy-Weinberg equilibrium. Allele frequencies for Ala49 and Thr49 in the patients were 71.9 and 28.1%, respectively, and those for both polymorphisms in the controls were 89.7 and 10.3%, respectively. We demonstrated a remarkable difference between the patients and controls for the Ala49Thr polymorphism (OR 2.4; CI 95% 1.2-4.9; p 0.004 <0.05). For the Thr49 allele, there was an obvious, significantly higher risk in the patients. For the SRD5A2 gene Val89Leu polymorphism, there was not any statistical difference (OR 1.2; CI 95% 0.8-1.8; p 0.248, p >0.05). The frequencies, according to our study, of the Val89 and Leu89 genotypes for patients and controls are shown in Table 4.

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