Methods for Identifying and Quantifying mRNA Expression of Androgen Receptor Splicing Variants in Prostate Cancer

2016 ◽  
pp. 165-177
Author(s):  
Yingming Li ◽  
Scott M. Dehm
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Mrna Expression ◽  
Splicing Variants

scholarly journals MP16-10 MIR-8080 RECRUITMENT INHIBITS EXPRESSION OF ANDROGEN RECEPTOR SPLICING VARIANTS IN CASTRATION-RESISTANT PROSTATE CANCER

2020 ◽  
Vol 203 ◽  
pp. e218
Author(s):  
Taku Naiki* ◽  
Aya Naiki-Ito ◽  
Hiroyuki Kato ◽  
Keitaro Iida ◽  
Toshiki Etani ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant ◽  
Splicing Variants

Abstract 1712: Androgen receptor splicing variants promote therapeutic resistance in prostate cancer

2010 ◽  
Author(s):  
Zhiyong Guo ◽  
Xi Yang ◽  
Feng Sun ◽  
Douglas E. Linn ◽  
Richeng Jiang ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Therapeutic Resistance ◽  
Splicing Variants

scholarly journals Emerging data on androgen receptor splice variants in prostate cancer

2016 ◽  
Vol 23 (12) ◽  
pp. T199-T210 ◽  
Author(s):  
Subing Cao ◽  
Yang Zhan ◽  
Yan Dong
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Splice Variants ◽  
Deep Understanding ◽  
Castration Resistant Prostate Cancer ◽  
Castration Resistant ◽  
Splicing Variants ◽  
Current Therapies ◽  
Alternatively Spliced ◽  
Androgen Receptor Splice Variants

Androgen receptor splice variants are alternatively spliced variants of androgen receptor, which are C-terminally truncated and lack the canonical ligand-binding domain. Accumulating evidence has indicated a significant role of androgen receptor splice variants in mediating resistance of castration-resistant prostate cancer to current therapies and in predicting therapeutic responses. As such, there is an urgent need to target androgen receptor splicing variants for more effective treatment of castration-resistant prostate cancer. Identification of precise and critical targeting points to deactivate androgen receptor splicing variants relies on a deep understanding of how they are generated and the mechanisms of their action. In this review, we will focus on the emerging data on their generation, clinical significance and mechanisms of action as well as the therapeutic influence of these findings.

scholarly journals Castration-Resistant Prostate Cancer Refractory to Second-Generation Androgen Receptor Axis-Targeted Agents: Opportunities and Challenges

Cancers ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 345 ◽  
Author(s):  
Yuki Kita ◽  
Takayuki Goto ◽  
Shusuke Akamatsu ◽  
Toshinari Yamasaki ◽  
Takahiro Inoue ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Second Generation ◽  
Considerable Proportion ◽  
Castration Resistant Prostate Cancer ◽  
Nonsense Mutations ◽  
Post Translational Modifications ◽  
Downstream Signaling ◽  
Castration Resistant ◽  
Splicing Variants

Second-generation androgen receptor axis-targeted (ARAT) agents, namely abiraterone and enzalutamide, enable stronger blockade of the androgen receptor (AR) axis and longer survival of men with castration-resistant prostate cancer (CRPC). However, the extent of the improved survival remains insufficient and the majority of patients eventually develop resistance to these novel agents. Some patients develop resistance against ARAT treatment through mechanisms termed “complete AR independence” or “AR indifference”, and no longer require activation of the AR axis. However, a considerable proportion of CRPC patients remain persistently dependent on AR or its downstream signaling pathways. Ligand-independent activation of the AR, an AR axis-dependent mechanism, is mediated by truncated forms of ARs that lack the ligand-binding domain (LBD), arising as products of AR splicing variants or nonsense mutations of AR. Post-translational modifications of ARs can also contribute to ligand-independent transactivation of the AR. Other mechanisms for AR axis activation are mediated by pathways that bypass the AR. Recent studies revealed that the glucocorticoid receptor can upregulate a similar transcription program to that of the AR, thus bypassing the AR. ARAT agents are essentially ineffective for CRPC driven by these AR-independent mechanisms. This review article describes recent efforts to overcome these refractory machineries for the development of next-generation AR axis blockade in CRPC.

Higher Tumor to Benign Ratio of the Androgen Receptor mRNA Expression Associates with Prostate Cancer Progression after Radical Prostatectomy

Urology ◽  
2007 ◽  
Vol 70 (6) ◽  
pp. 1225-1229 ◽  
Author(s):  
Inger L. Rosner ◽  
Lakshmi Ravindranath ◽  
Bungo Furusato ◽  
Yongmei Chen ◽  
Chunling Gao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Radical Prostatectomy ◽  
Mrna Expression ◽  
Cancer Progression ◽  
Prostate Cancer Progression ◽  
Receptor Mrna

Identification of novel truncated androgen receptor (AR) mutants including unreported pre-mRNA splicing variants in the 22Rv1 hormone-refractory prostate cancer (PCa) cell line

2010 ◽  
Vol 31 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Gemma Marcias ◽  
Eva Erdmann ◽  
Gaëlle Lapouge ◽  
Christelle Siebert ◽  
Philippe Barthélémy ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Cell Line ◽  
Mrna Splicing ◽  
Hormone Refractory Prostate Cancer ◽  
Splicing Variants ◽  
Hormone Refractory
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