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Merging Absolute and Relative Quantitative PCR Data to Quantify STAT3 Splice Variant Transcripts
Published on: October 9, 2016
Splicing variants of androgen receptor in prostate cancer
Haitao Zhang1, Yang Zhan2, Xichun Liu3
1Department of Pathology and Laboratory Medicine, Tulane University School of Medicine New Orleans, LA ; Department of Tulane Cancer Center New Orleans, LA.
Abstract:
Significant advances in our understanding of continued androgen receptor (AR) signaling in castration-resistant prostate cancer have led to the development and FDA approval of two next-generation androgen-directed therapies, abiraterone and enzalutamide. These new therapies heralded a new era of prostate cancer therapy. However, disease progression during androgen-directed therapies remains the most critical challenge in the clinical management of prostate cancer. Accumulating evidence points to an important contribution of constitutively-active AR splice variants to AR-driven tumor progression during androgen-directed therapies. In this review, we will focus on the structure, activity, detection, clinical relevance, and mechanisms of production of AR splice variants.
Insights
Androgen receptor splice variants drive castration-resistant prostate cancer progression despite new therapies like abiraterone and enzalutamide. Understanding AR variants is key to overcoming treatment resistance in prostate cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Castration-resistant prostate cancer (CRPC) remains a clinical challenge.
- Androgen receptor (AR) signaling persists in CRPC.
- New therapies (abiraterone, enzalutamide) target AR but resistance develops.
Purpose of the Study:
- To review the role of AR splice variants in CRPC progression.
- To discuss the structure, activity, detection, and clinical relevance of AR variants.
- To explore mechanisms of AR variant production.
Main Methods:
- Literature review of studies on AR splice variants in prostate cancer.
- Analysis of data on AR variant structure and function.
- Examination of clinical studies investigating AR variants and treatment outcomes.
Main Results:
- Constitutively active AR splice variants contribute to AR-driven tumor progression.
- AR variants are detected in CRPC and associated with treatment resistance.
- Mechanisms of AR variant production are increasingly understood.
Conclusions:
- AR splice variants are critical drivers of treatment resistance in CRPC.
- Targeting AR variants may offer new therapeutic strategies.
- Further research into AR variant biology is essential for improving CRPC management.
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