Recurrent gene fusions in prostate cancer

被引:525
作者
Kumar-Sinha, Chandan [1 ,5 ]
Tomlins, Scott A. [1 ,5 ]
Chinnaiyan, Arul M. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Dept Pathol, Ann Arbor, MI USA
[2] Howard Hughes Med Inst, Ann Arbor, MI USA
[3] Univ Michigan, Dept Urol, Sch Med, Ann Arbor, MI 48109 USA
[4] Univ Michigan, Ctr Comprehens Canc, Sch Med, Ann Arbor, MI 48109 USA
[5] Michigan Ctr Translat Pathol, Ann Arbor, MI 48109 USA
关键词
D O I
10.1038/nrc2402
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The discovery of recurrent gene fusions in a majority of prostate cancers has important clinical and biological implications in the study of common epithelial tumours. Gene fusion and chromosomal rearrangements were previously thought to be primarily the oncogenic mechanism of haematological malignancies and sarcomas. The prostate cancer gene fusions that have been identified thus far are characterized by 5' genomic regulatory elements, most commonly controlled by androgen, fused to members of the Ets family of transcription factors, leading to the overexpression of oncogenic transcription factors. Ets gene fusions probably define a distinct class of prostate cancer, and this might have a bearing on diagnosis, prognosis and rational therapeutic targeting.
引用
收藏
页码:497 / 511
页数:15
相关论文
共 125 条
[1]   THE C-MYC ONCOGENE DRIVEN BY IMMUNOGLOBULIN ENHANCERS INDUCES LYMPHOID MALIGNANCY IN TRANSGENIC MICE [J].
ADAMS, JM ;
HARRIS, AW ;
PINKERT, CA ;
CORCORAN, LM ;
ALEXANDER, WS ;
CORY, S ;
PALMITER, RD ;
BRINSTER, RL .
NATURE, 1985, 318 (6046) :533-538
[2]  
Afar DEH, 2001, CANCER RES, V61, P1686
[3]   Frequent engagement of the classical and alternative NF-κB pathways by diverse genetic abnormalities in multiple myeloma [J].
Annunziata, Christina M. ;
Davis, R. Eric ;
Demchenko, Yulia ;
Bellamy, William ;
Gabrea, Ana ;
Zhan, Fenghuang ;
Lenz, Georg ;
Hanamura, Ichiro ;
Wright, George ;
Xiao, Wenming ;
Dave, Sandeep ;
Hurt, Elaine M. ;
Tan, Bruce ;
Zhao, Hong ;
Stephens, Owen ;
Santra, Madhumita ;
Williams, David R. ;
Dang, Lenny ;
Barlogie, Bart ;
Shaughnessy, John D., Jr. ;
Kuehl, W. Michael ;
Staudt, Louis M. .
CANCER CELL, 2007, 12 (02) :115-130
[4]  
[Anonymous], CANC FACTS FIG 2007
[5]   Heterogeneity of gleason grade in multifocal adenocarcinorna of the prostate [J].
Arora, R ;
Koch, MO ;
Eble, JN ;
Ulbright, TM ;
Li, L ;
Cheng, L .
CANCER, 2004, 100 (11) :2362-2366
[6]   Duplication of the fusion of TMPRSS2 to ERG sequences identifies fatal human prostate cancer [J].
Attard, G. ;
Clark, J. ;
Ambroisine, L. ;
Fisher, G. ;
Kovacs, G. ;
Flohr, P. ;
Berney, D. ;
Foster, C. S. ;
Fletcher, A. ;
Gerald, W. L. ;
Moller, H. ;
Reuter, V. ;
De Bono, J. S. ;
Scardino, P. ;
Cuzick, J. ;
Cooper, C. S. .
ONCOGENE, 2008, 27 (03) :253-263
[7]   TMPRSS2-ERG fusion heterogeneity in Multifocal prostate cancer: Clinical and biologic implications [J].
Barry, Marc ;
Perner, Sven ;
Demichelis, Francesca ;
Rubin, Mark A. .
UROLOGY, 2007, 70 (04) :630-633
[8]   Estrogen receptor expression in prostate cancer and premalignant prostatic lesions [J].
Bonkhoff, H ;
Fixemer, T ;
Hunsicker, I ;
Remberger, K .
AMERICAN JOURNAL OF PATHOLOGY, 1999, 155 (02) :641-647
[9]   ETV1 is a novel androgen receptor-regulated gene that mediates prostate cancer cell invasion [J].
Cai, Changmeng ;
Hsieh, Chen-Lin ;
Omwancha, Josephat ;
Zheng, Zhe ;
Chen, Shao-Yong ;
Baert, Jean-Luc ;
Shemshedini, Lirim .
MOLECULAR ENDOCRINOLOGY, 2007, 21 (08) :1835-1846
[10]   TMPRSS2-ERG gene fusion causing ERG overexpression precedes chromosome copy number changes in prostate carcinomas and paired HGPIN lesions [J].
Cerveira, Nuno ;
Ribeiro, Franclim R. ;
Peixoto, Ana ;
Costa, Vera ;
Henrique, Rui ;
Jeronimo, Carmen ;
Teixeira, Manuel R. .
NEOPLASIA, 2006, 8 (10) :826-832