Clonal origin and spread of metastatic prostate cancer

被引:31
|
作者
van Etten, Jamie L. [1 ]
Dehm, Scott M. [1 ,2 ,3 ]
机构
[1] Univ Minnesota, Mason Canc Ctr, Minneapolis, MN USA
[2] Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA
[3] Univ Minnesota, Dept Urol, Minneapolis, MN USA
关键词
metastasis; prostate; endocrine therapy resistance; cell lineage/genetics; clonal spread; COPY-NUMBER ANALYSIS; ACTIVE ANDROGEN RECEPTOR; MUTATIONAL LANDSCAPE; MOLECULAR ANALYSIS; MONOCLONAL ORIGIN; SPLICE VARIANTS; HETEROGENEITY; EVOLUTION; PROGRESSION; RESISTANCE;
D O I
10.1530/ERC-16-0049
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Metastatic disease is responsible for the majority of prostate cancer deaths. The standard treatment for metastatic disease is surgical or chemical castration in the form of androgen deprivation therapy. Despite initial success and disease regression, resistance to therapy ultimately develops and the disease transitions to castration-resistant prostate cancer, which is uniformly fatal. Thus, developing an understanding of genetic evolution in metastasis and in response to therapy has been a focus of recent studies. Large-scale sequencing studies have provided an expansive catalog of the mutation events that occur in the prostate cancer genome at various stages of disease progression. Small-scale studies have interrogated the genomic composition of multiple metastatic sites within individual patients or have tracked clonal evolution longitudinally in tissues, circulating tumor cells, or circulating tumor DNA. Collectively, these efforts have provided a new conceptual framework for understanding the origin of prostate cancer, as well as the origin and evolution of metastatic disease. In this review, we highlight these recent insights into the spatiotemporal landscape of genetic evolution of prostate cancer.
引用
收藏
页码:R207 / R217
页数:11
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