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Updated: Feb 11, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Androgen action in prostate function and disease.

Partha P Banerjee1, Subhadra Banerjee2, Terry R Brown3

  • 1Department of Biochemistry, Molecular and Cellular Biology, Georgetown University Medical CenterWashington, DC 20057, USA.

American Journal of Clinical and Experimental Urology
|April 19, 2018
PubMed
Summary
This summary is machine-generated.

Benign prostatic hyperplasia (BPH) and prostate cancer (CaP) involve androgens, but their exact roles are unclear. Understanding prostate cell plasticity is key to treating castration-resistant prostate cancer (CRPC).

Keywords:
BPHCRPCLeydig cellProstateagingandrogens

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Area of Science:

  • Urology
  • Endocrinology
  • Oncology

Background:

  • Benign prostatic hyperplasia (BPH) and prostate cancer (CaP) are common in aging men.
  • Androgens are crucial for prostate function, but their precise role in BPH and CaP etiology is not fully established.
  • Age-related decreases in testosterone occur alongside increased BPH incidence.

Purpose of the Study:

  • To explore the roles of androgens, estrogens, and growth factors in BPH.
  • To investigate the mechanisms behind prostate cancer development and resistance to androgen deprivation therapy.
  • To understand the plasticity and heterogeneity of prostate epithelial cells in castration-resistant prostate cancer (CRPC).

Main Methods:

  • Review of existing literature on BPH and CaP.
  • Analysis of the roles of androgens and other factors in prostate hyperplasia.
  • Examination of cellular responses to androgen ablation in prostate cancer models.

Main Results:

  • Androgens, estrogens, and growth factors contribute to BPH, though the exact cause remains unknown.
  • Androgen deprivation therapy is effective for advanced prostate cancer but often leads to resistance.
  • Prostate cancer cells exhibit plasticity, potentially leading to androgen receptor-positive and negative populations in CRPC.

Conclusions:

  • Further research is needed to clarify the exact etiology of BPH and CaP.
  • Understanding prostate epithelial cell plasticity is essential for developing effective strategies against CRPC.
  • Targeting cellular heterogeneity may offer new therapeutic avenues for advanced prostate cancer.