Castagnaro M, Yandell D W, Dockhorn-Dworniczak B, Wolfe H J, Poremba C
Department of Pathology, New England Medical Center, Boston.
Verh Dtsch Ges Pathol. 1993;77:119-23.
One of the most interesting but still unsolved issues in prostate cancer is the role of androgens, the androgen receptor (AR) and the p53 tumor suppressor gene in the development and/or progression of prostatic neoplasia. DNA obtained from prostate tissues of 7 normal donors, 5 BPH and 10 adenocarcinomas at different stages was amplified by the polymerase-chain-reaction (PCR). The products were analysed by single strand conformation polymorphism (SSCP), and by direct sequencing of those that displayed altered electrophoretic behavior. The molecular analysis of exons 1 to 8 of the AR gene revealed point mutations in codons 340 (exon 1) and 798 (exon 6) in 2/10 prostate carcinomas. No mutations were found in the p53 gene. Our findings suggest that mutations of the AR gene are relatively frequent in prostate cancer and may have therapeutical significance.
前列腺癌中最有趣但仍未解决的问题之一是雄激素、雄激素受体（AR）和p53肿瘤抑制基因在前列腺肿瘤发生和/或进展中的作用。从7名正常供体、5例良性前列腺增生（BPH）和10例不同阶段腺癌的前列腺组织中提取的DNA，通过聚合酶链反应（PCR）进行扩增。产物通过单链构象多态性（SSCP）分析，并对那些电泳行为改变的产物进行直接测序。AR基因外显子1至8的分子分析显示，在10例前列腺癌中有2例在密码子340（外显子1）和798（外显子6）处发生点突变。在p53基因中未发现突变。我们的研究结果表明，AR基因的突变在前列腺癌中相对常见，可能具有治疗意义。
