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Related Concept Videos

Metastasis02:30

Metastasis

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Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
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...
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Related Experiment Video

Updated: Nov 1, 2025

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

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[Metastatic castration-resistant prostate cancer].

Vanessa Henriques1, Mike Wenzel2,3, Melanie-Christin Demes4

  • 1Senckenbergisches Institut für Pathologie, Universitätsklinikum Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt/M., Deutschland. vanessa.smh@gmail.com.

Der Pathologe
|June 25, 2021
PubMed
Summary

Metastatic castration-resistant prostate cancer (mCRPC) has limited treatment options. Recent pathology findings, including BRCA1/2 mutations and AR-V7, offer new avenues for personalized therapies in advanced prostate cancer.

Keywords:
Androgen receptorBRCA1 geneBRCA2 geneIpatasertibPoly(ADP-ribose) polymerase inhibitors

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Area of Science:

  • Oncology
  • Pathology
  • Genetics

Background:

  • Metastatic castration-resistant prostate cancer (mCRPC) represents an advanced stage with few therapeutic choices.
  • Understanding the molecular landscape of mCRPC is crucial for developing effective treatments.

Purpose of the Study:

  • To review recent histopathologic and molecular findings in mCRPC.
  • To explore how these findings can guide novel, individualized therapies.

Main Methods:

  • Review of current literature on histopathologic and molecular alterations in mCRPC.
  • Analysis of specific biomarkers such as BRCA1/2 mutations, AR-V7, PTEN deletion, and t-NEPC.

Main Results:

  • Pathogenic mutations in DNA repair genes (BRCA1/2) are significant in mCRPC.
  • Androgen receptor splice variant 7 (AR-V7) is a key biomarker.
  • PTEN tumor suppressor gene deletion and treatment-emergent neuroendocrine prostate cancer (t-NEPC) are emerging concerns.

Conclusions:

  • Pathology plays an increasingly vital role in guiding therapy for mCRPC.
  • Identified molecular and histopathologic changes provide a basis for developing targeted and personalized treatment strategies.