ArticleBritish journal of cancer2018
Constitutively active androgen receptor splice variants AR-V3, AR-V7 and AR-V9 are co-expressed in castration-resistant prostate cancer metastases.
Article in British journal of cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 3 of them syntheses that pooled it.
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Who cites it
54 citing papers in PubMed, 3 syntheses or guidelines pooled it, 90 citations in OpenAlex.
- The positive relationship between androgen receptor splice variant-7 expression and the risk of castration-resistant prostate cancer: A cumulative analysis.Frontiers in oncology · 2023Pooled it
- The promising role of new molecular biomarkers in prostate cancer: from coding and non-coding genes to artificial intelligence approaches.Prostate cancer and prostatic diseases · 2022Pooled it
- Androgen receptor variant-driven prostate cancer II: advances in laboratory investigations.Prostate cancer and prostatic diseases · 2020Pooled it
- Citron kinase activity controls alternative splicing events that drive prostate cancer growth.Science advances · 2026Article
- From fragments to full pictures: how long-read sequencing platforms are revolutionizing oncology research.Molecular biology reports · 2026Review
- Molecular determinants of AR-enhancer interaction and cistrome reprogramming in prostate cancer progression.Endocrine-related cancer · 2026Review
- HDAC11 Regulates RNA Splicing via De-Fatty Acylation of SF3B2.bioRxiv : the preprint server for biology · 2026Article
- Androgen receptor reactivation in castration-resistant prostate cancer: mechanisms, epigenetic adaptation, and therapeutic vulnerabilities.Frontiers in oncology · 2026Review
- Androgen receptor splice variant expression and prostate cancer recurrence after salvage therapy.NPJ precision oncology · 2025Article
- Molecular analysis of androgen receptor splice variant AR-V3 reveals eminent ambiguity regarding activity and clinical utility.Cancer cell international · 2025Article
- Article
- The MicroRNA miR-454 and the mediator complex component MED12 are regulators of the androgen receptor pathway in prostate cancer.Scientific reports · 2025Article
- Androgen receptor inhibitors in treating prostate cancer.Asian journal of andrology · 2025Review
- Unlocking artificial intelligence, machine learning and deep learning to combat therapeutic resistance in metastatic castration-resistant prostate cancer: a comprehensive review.Ecancermedicalscience · 2025Review
- Androgen receptor activation promotes tumor progression in canine and human triple negative breast cancer cell lines.Frontiers in veterinary science · 2025Article
- Article
- Assessing the Potential of Small Peptides for Altering Expression Levels of the Iron-Regulatory GenesInternational journal of molecular sciences · 2023Article
- Long-range gene regulation in hormone-dependent cancer.Nature reviews. Cancer · 2023Review
- BRCA-deficient metastatic prostate cancer has an adverse prognosis and distinct genomic phenotype.EBioMedicine · 2023Article
- Symphony in the crowd: Key genetic alterations in prostate cancer.Cancer innovation · 2023Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundA significant subset of prostate cancer (PC) patients with a castration-resistant form of the disease (CRPC) show primary resistance to androgen receptor (AR)-targeting drugs developed against CRPC. As one explanation could be the expression of constitutively active androgen receptor splice variants (AR-Vs), our current objectives were to study AR-Vs and other AR aberrations to better understand the emergence of CRPC.
methodsWe analysed specimens from different stages of prostate cancer by next-generation sequencing and immunohistochemistry.
resultsAR mutations and copy number variations were detected only in CRPC specimens. Genomic structural rearrangements of AR were observed in 5/30 metastatic CRPC patients, but they were not associated with expression of previously known AR-Vs. The predominant AR-Vs detected were AR-V3, AR-V7 and AR-V9, with the expression levels being significantly higher in CRPC cases compared to prostatectomy samples. Out of 25 CRPC metastases that expressed any AR variant, 17 cases harboured expression of all three of these AR-Vs. AR-V7 protein expression was highly heterogeneous and higher in CRPC compared to hormone-naïve tumours.
conclusionsAR-V3, AR-V7 and AR-V9 are co-expressed in CRPC metastases highlighting the fact that inhibiting AR function via regions common to all AR-Vs is likely to provide additional benefit to patients with CRPC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.