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Updated: Apr 19, 2026

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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
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[Current status of castration resistant prostate cancer basic research].
Nihon Rinsho. Japanese Journal of Clinical Medicine
|December 19, 2014
Summary
Novel therapies highlight the importance of androgen pathways in castration-resistant prostate cancer (CRPC). Research explores AR alterations, gene fusions like TMPRSS2-ERG, and miRNA regulation in CRPC progression.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Context:
- Recent advancements in anti-androgen therapies and CYP-17 inhibitors have renewed focus on androgen signaling in castration-resistant prostate cancer (CRPC).
- Understanding the molecular mechanisms driving CRPC is crucial for developing effective treatments.
Purpose:
- To review classical and emerging topics in the basic research of castration-resistant prostate cancer.
- To highlight key molecular alterations and regulatory pathways involved in CRPC development.
Summary:
- Castration resistance in prostate cancer is driven by androgen receptor (AR) amplification, mutations, and splicing variants leading to ligand-independent activation.
- Novel AR regulation mechanisms include chromosomal rearrangements involving FOXA and the prevalent TMPRSS2-ERG gene fusion.
- Non-coding microRNAs (miRNAs) also play a significant role in AR-mediated oncogenic pathways in CRPC.
Impact:
- This review provides a comprehensive overview of current research frontiers in CRPC.
- It aids researchers in understanding the complex molecular landscape of CRPC.
- Informs the development of targeted therapies for advanced prostate cancer.
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