Nupponen N, Visakorpi T
Laboratory of Cancer Genetics, Institute of Medical Technology, University of Tampere, and Tampere University Hospital, Finland.
Eur Urol. 1999;35(5-6):351-4. doi: 10.1159/000019907.
Despite the clinical importance of prostate cancer, the molecular mechanisms underlying the development and progression of prostate cancer are poorly understood. The lack of knowledge on the mechanisms has probably been one of the most important reasons why no new treatment modalities have been developed to cure the disease. Recent studies, especially those performed by comparative genomic hybridization, have revealed the frequent chromosomal alterations that most likely harbor the genes critical for the progression of prostate cancer. Such genetic aberrations include losses of 8p, 10q, 16q, and 13q as well as gains of 7p, 7q, 8q, and Xq. Unfortunately, the target genes for these alterations are, in most of the cases, not known. We have recently identified the androgen receptor (AR) gene as a target gene for the Xq12 amplification found in one-third of the hormone-refractory prostate cancer. The findings suggest that the AR gene amplification and overexpression is involved in the emergence of hormone-refractory prostate cancer.
尽管前列腺癌具有临床重要性，但其发生和进展的分子机制仍知之甚少。对这些机制缺乏了解可能是尚未开发出治愈该疾病的新治疗方法的最重要原因之一。最近的研究，尤其是那些通过比较基因组杂交进行的研究，揭示了频繁的染色体改变，这些改变很可能包含对前列腺癌进展至关重要的基因。此类基因畸变包括8p、10q、16q和13q的缺失以及7p、7q、8q和Xq的增加。不幸的是，在大多数情况下，这些改变的靶基因尚不清楚。我们最近将雄激素受体（AR）基因鉴定为在三分之一的激素难治性前列腺癌中发现的Xq12扩增的靶基因。这些发现表明，AR基因扩增和过表达与激素难治性前列腺癌的出现有关。
