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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。
Objective: To study the mechanism of the mutation and deletion of tumor suppressor gene CDKN2 in the etiopathogenisis of human benign prostatic hyperplasia (BPH). Methods: The homozygous deletions and mutations of CDKN2 gene in 20 cases of normal prostate tissue and 41 cases of BPH were analyzed by PCR-silver staining with SSCP technique. Results: The deletion of CDKN2 gene was found in 13 cases of BPH, with a total deletion rate of 31.6%: one case of normal prostate tissue had deletion of CDKN2 gene, a deletion rate of 5% (P <0.05), and no mutation of CDKN2 gene. Conclusion: The variation of CDKN2 gene is related to the pathogenesis of BPH. Homozygous deletion is one of the main mechanisms of CDKN2 in prostatic hyperplasia.