机构:
Dept Pathol, Ann Arbor, MI USA
Michigan Ctr Translat Pathol, Ann Arbor, MI 48109 USADept Pathol, Ann Arbor, MI USA
Kumar-Sinha, Chandan
[1
,5
]
Tomlins, Scott A.
论文数: 0引用数: 0
h-index: 0
机构:
Dept Pathol, Ann Arbor, MI USA
Michigan Ctr Translat Pathol, Ann Arbor, MI 48109 USADept Pathol, Ann Arbor, MI USA
Tomlins, Scott A.
[1
,5
]
Chinnaiyan, Arul M.
论文数: 0引用数: 0
h-index: 0
机构:
Dept Pathol, Ann Arbor, MI USA
Howard Hughes Med Inst, Ann Arbor, MI USA
Univ Michigan, Dept Urol, Sch Med, Ann Arbor, MI 48109 USA
Univ Michigan, Ctr Comprehens Canc, Sch Med, Ann Arbor, MI 48109 USA
Michigan Ctr Translat Pathol, Ann Arbor, MI 48109 USADept Pathol, Ann Arbor, MI USA
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
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.