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Updated: Jun 21, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Pathogenesis of prostate cancer and hormone refractory prostate cancer
J S Girling1, H C Whitaker, I G Mills
1CRUK Uro-oncolgy Group, Department of Oncology, University of Cambridge, Hutchison/MRC Research Centre, Cambridge, CB2 2XZ, UK.
Abstract:
Prostate cancer is the second most common malignancy in males and the leading cause of cancer death. Prostate cancer is initially androgen dependent and relies upon the androgen receptor (AR) to mediate the effects of androgens. The AR is also the target for therapy using antiandrogens and LHRH analogues. However, all cancers eventually become androgen independent, often referred to as hormone refractory prostate cancer. The processes involved in this transformation are yet to be fully understood but research in this area has discovered numerous potential mechanisms including AR amplification, over-expression or mutation and alterations in the AR signaling pathway. This review of the recent literature examines the current knowledge and developments in the understanding of the molecular biology of prostate cancer and hormone refractory prostate cancer, summarizing the well characterized pathways involved as well as introducing new concepts that may offer future solutions to this difficult problem.
Insights
Prostate cancer initially depends on androgens but becomes hormone-refractory. Understanding androgen receptor (AR) pathway changes is key to treating advanced prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Urology
Background:
- Prostate cancer is a leading cause of cancer death in males.
- It is initially androgen-dependent, relying on the androgen receptor (AR).
- Hormone-refractory prostate cancer (HRPC) develops as cancers become androgen-independent.
Purpose of the Study:
- To review current knowledge on the molecular biology of prostate cancer.
- To examine developments in understanding hormone-refractory prostate cancer.
- To summarize known pathways and introduce novel concepts for HRPC.
Main Methods:
- Literature review of recent research.
- Analysis of molecular mechanisms in prostate cancer progression.
- Synthesis of information on AR signaling pathways.
Main Results:
- Identified AR amplification, over-expression, and mutation as mechanisms in HRPC.
- Highlighted alterations in the AR signaling pathway.
- Summarized well-characterized and emerging pathways.
Conclusions:
- Understanding the molecular basis of HRPC is crucial for developing new therapies.
- Further research into AR pathway alterations may offer future solutions.
- This review consolidates current knowledge and points to future research directions.
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