Clonal origin and spread of metastatic prostate cancer

Jamie L. Van Etten, Scott M. Dehm

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)R207-R217
JournalEndocrine-related cancer
Issue number4
StatePublished - Apr 2016

Bibliographical note

Funding Information:
S M D is currently funded by a 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 grants W81XWH-12-2-0093, W81XWH-13-1-0518, W81XWH-15-1-0633, and W81XWH-15-1-0501; and a grant from the Minnesota Partnership for Biotechnology and Medical Genomics.J L V is supported by the Cancer Biology Training Grant T32 CA009138

Publisher Copyright:
© 2016 Society for Endocrinology.


  • Cell lineage/genetics
  • Clonal spread
  • Endocrine therapy resistance
  • Metastasis
  • Prostate


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