CDKN2基因的变异在人前列腺增生症中发病机制的研究

Alteration of CDKN2/p16 gene in human benign prostatic hyperplasia

目的：研究抑癌基因CDKN2的突变、缺失在人前列腺增生症（BPH）病因中的作用机制。方法：用PCR-银染SSCP技术分析了20例正常前列腺组织和41例BPH中CDKN2基因纯合性缺失和突变的情况。结果：13例BPH有CDKN2基因缺失，总缺失率为31.6％：正常前列腺组织中有1例出现CDKN2基因缺失.缺失率为5％（P＜0.05）;无CDKN2基因的突变。结论：CDKN2基因的变异与BPH的发病机制有关，纯合性缺失是CDKN2基因在前列腺增生中主要灭活机制之一。

Objectives: To study the role of CDKN2 gene alteration in the BPH pathogenesis. Methods: Forty-one BPH and 20 normal prostrate tissue were examined for CDKN2 gene deletion and mutation using PCR--SSCP. Results: Homozygous deletion of CDKN2 gene in 13(31. 6% ) BPH and 1 (5%) normal prostate tissue were founded (PM 0. 05 ). There was no mutation in BPH. Conclusions:CDKN2 gene played an important role in the proliferation of BPH. Homozygous deletion was one of major inactivation mechanisms of CDKN2 gene in BPH.