Analysis of the polymorphism in the androgen receptor gene of BPH patients

1998 Fiscal Year Final Research Report Summary

• Project/Area Number: 09671626
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Urology
• Research Institution: KYOTO UNIVERSITY
• Principal Investigator: TERAI Akito Kyoto University, Urology, Instructor, 医学研究科, 助手 (50243019)
• Co-Investigator(Kenkyū-buntansha): KAMOTO Toshiyuki Kyoto University, Urology, Instructor, 医学研究科, 助手 (00281098) ; SHICHIRI Yasumasa Kyoto University, Urology, Instructo, 医学研究科, 助手 (20263080) ; MIZUTANI Yoichi Kyoto University, Urology, Instructo, 医学研究科, 助手 (10243031) ; KAKEHI Yoshiyuki Kyoto University, Urology, Assistant professo, 医学研究科, 講師 (20214273)
• Project Period (FY): 1997 – 1998
• Keywords: Benign prostatic hyperplasia / Androgen receptor / polymorphism

Research Abstract

The androgen receptor (AR) gene contains a polymorphic CAG microsatellite. Previous studies showed that the length of the CAG repeat correlates inversely with transcriptional activity of the AR and the short CAG repeat length might be associated with the increased risk of the prostate cancer. The purpose of the present study was to evaluate an association between the growth of hyperplastic adenoma and the CAG repeat lengths in AR gene.
We examined 252 patients who underwent prostatectomy and had the pathological diagnosis of BPH by the step section. Furthermore, we examined 41 controls (>65 year old) with the prostate smaller than 20ml and with normal serum PSA level. CAG repeat length was inversely related to the weight of adenomas in the prostatectomized patients. The mean repeats length for the larger (*64 g : mean+0.8SD), smaller (24 g : mean-0.8SD) adenoma subgroup and the control group were 21.7*2.9 and 2.8*2.2 and 23.12.4, respectively. The larger adenoma subgroup tended to have shorter CAG repeat length than either smaller adenoma subgroup or control group (p<0.05 and p<0.02, respectively), For the patient with <23 CAG repeats, the relative risk developing the larger adenoma was statistically significant (Relative risk ; 2.83.95% confidence interval ; 1.21-6.61). All cases with *17 CAG repeats had the larger adenomas. In summary, our results suggested that short CAG repeats of the androgen receptor gene might have the promoting influence on the growth of the prostatic hyperplasia as one of the genetic factors.