Clinical variability and molecular heterogeneity in prostate cancer

被引：94

作者：

Shoag, Jonathan ^{[1
]}

Barbieri, Christopher E. ^{[1
,2
]}

机构：

[1] Weill Cornell Med Coll, NewYork Presbyterian Hosp, Dept Urol, New York, NY 10065 USA

[2] Weill Cornell Med Coll, Sandra & Edward Meyer Canc Ctr, New York, NY 10065 USA

来源：

ASIAN JOURNAL OF ANDROLOGY | 2016年 / 18卷 / 04期

关键词：

cell biology; ERG; genomics; molecular heterogeneity; prostate cancer; sequencing; serine peptidase inhibitor; Kazal type 1; SPOP; tumor profiling; LYMPH-NODE DISSECTION; ETS GENE FUSIONS; ERG REARRANGEMENT; INTRAEPITHELIAL NEOPLASIA; MUTATIONAL LANDSCAPE; ANDROGEN RECEPTOR; TUMOR-CELLS; TMPRSS2-ERG; SPOP; PTEN;

D O I：

10.4103/1008-682X.178852

中图分类号：

R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

摘要：

Prostate cancer is a clinically heterogeneous disease, with some men having indolent disease that can safely be observed, while others have aggressive, lethal disease. Over the past decade, researchers have begun to unravel some of the genomic heterogeneity that contributes to these varying clinical phenotypes. Distinct molecular sub-classes of prostate cancer have been identified, and the uniqueness of these sub-classes has been leveraged to predict clinical outcomes, design novel biomarkers for prostate cancer diagnosis, and develop novel therapeutics. Recent work has also elucidated the temporal and spatial heterogeneity of prostate cancer, helping us understand disease pathogenesis, response to therapy, and progression. New genomic techniques have provided us with a window into the remarkable clinical and genomic heterogeneity of prostate cancer, and this new perspective will increasingly impact patient care.

引用

页码：543 / 548

页数：6

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