Chromosomal aberrations in prostate cancer

被引:32
作者
Saramaki, Outi
Visakorpi, Tapio [1 ]
机构
[1] Univ Tampere, Inst Med Technol, FI-33014 Tampere, Finland
[2] Tampere Univ Hosp, Tampere, Finland
来源
FRONTIERS IN BIOSCIENCE-LANDMARK | 2007年 / 12卷
关键词
prostate carcinoma; chromosomal alterations; neoplasia; amplification; deletion; chromosome; review;
D O I
10.2741/2312
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Prostate cancer incidence is steadily increasing in Western industrialized countries where it has become the most common male malignancy and second most common cause of cancer death among men. Despite efforts to understand the mechanisms of prostate cancer development and progression, the reasons for the disease remain unclear. Although recurrent DNA copy number aberrations in prostate cancer have been well documented in the past 15 years, most of the target genes for these aberrations remain to be identified. The most common DNA copy number aberrations are losses in chromosomes 5q, 6q, 8p, 10q, 13q, 16q, 17p, and 18q, and gains in 7p/ q, 8q, 9p, and Xq. In addition, a chromosomal rearrangement in 21q has been observed in over 50% of prostate cancers. The target genes for two common chromosomal aberrations have been identified: the androgen receptor ( AR) gene at Xq12, and TMPRSS2 and ERG at 21q. Putative target genes for other copy number aberrations include: NKX3-1 ( 8p loss), PTEN and MXI1 ( 10q loss), FOXO1A ( 13q loss), CDH1 and ATBF1 ( 16q loss), MCM7 and EZH2 ( 7q gain), TCEB1, EIF3S3 and MYC ( 8q gain). The identification of target genes for the chromosomal aberrations will provide new prognostic markers and therapeutic targets for future drug development.
引用
收藏
页码:3287 / 3301
页数:15
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