期刊
ENDOCRINE-RELATED CANCER
卷 23, 期 4, 页码 R207-R217出版社
BIOSCIENTIFICA LTD
DOI: 10.1530/ERC-16-0049
关键词
metastasis; prostate; endocrine therapy resistance; cell lineage/genetics; clonal spread
资金
- Movember/Prostate Cancer Foundation Challenge Award
- American Cancer Society Research Scholar Grant [RSG-12-031-01-TBE]
- NIH grant [R01CA174777]
- US Department of Defense Prostate Cancer Research Program [W81XWH-12-2-0093, W81XWH-13-1-0518, W81XWH-15-1-0633, W81XWH-15-1-0501]
- Minnesota Partnership for Biotechnology and Medical Genomics
- Cancer Biology Training Grant [T32 CA009138]
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.
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