Related Experiment Video
Updated: Mar 23, 2026
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Clonal origin and spread of metastatic prostate cancer
Jamie L Van Etten1, Scott M Dehm2
1Masonic Cancer CenterUniversity of Minnesota, Minneapolis, MN, USA.
Abstract:
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.
Insights
Prostate cancer deaths stem from metastasis. Understanding the genetic evolution of prostate cancer and its resistance to androgen deprivation therapy is crucial for developing new treatments.
Area of Science:
- Oncology
- Genetics
- Cancer Biology
Background:
- Metastatic prostate cancer is a leading cause of cancer death.
- Androgen deprivation therapy (ADT) is the standard treatment, but resistance develops, leading to fatal castration-resistant prostate cancer.
- Understanding the genetic basis of prostate cancer metastasis and therapy resistance is critical.
Purpose of the Study:
- To review recent insights into the genetic evolution of prostate cancer.
- To highlight the spatiotemporal landscape of genetic changes during prostate cancer progression and metastasis.
- To provide a framework for understanding the origins and evolution of metastatic disease.
Main Methods:
- Analysis of large-scale genome sequencing studies cataloging mutations in prostate cancer.
- Review of small-scale studies examining genomic composition across multiple metastatic sites.
- Integration of longitudinal studies tracking clonal evolution in tissues, circulating tumor cells, and circulating tumor DNA.
Main Results:
- Extensive catalogs of mutation events across various stages of prostate cancer progression are available.
- Genomic heterogeneity exists across different metastatic sites within individual patients.
- Longitudinal tracking reveals dynamic clonal evolution in response to therapy.
Conclusions:
- Recent genomic studies offer a new conceptual framework for prostate cancer origins and metastatic evolution.
- Understanding the spatiotemporal genetic landscape is key to deciphering treatment resistance.
- Further research into genetic evolution will inform future therapeutic strategies against metastatic prostate cancer.
Related Concept Videos
02:30Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
02:30Metastasis
02:07Tumor Progression
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
02:21Cancers Originate from Somatic Mutations in a Single Cell
02:18Cancer