ReviewNature reviews. Clinical oncology2018
Alternative splicing in prostate cancer.
Review in Nature reviews. Clinical oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
123 citing papers in PubMed, 181 citations in OpenAlex.
- Gankyrin-mediated interaction between cancer cells and tumor-associated macrophages facilitates prostate cancer progression and androgen deprivation therapy resistance.Oncoimmunology · 2023Trial
- Nivolumab plus ipilimumab, with or without enzalutamide, in AR-V7-expressing metastatic castration-resistant prostate cancer: A phase-2 nonrandomized clinical trial.The Prostate · 2021Trial
- Targeting the Androgen Receptor and Associated Cofactors in Prostate Cancer: Novel Approaches and Future Perspectives.International journal of molecular sciences · 2026Review
- A truncated TNS3 isoform expressed in metastatic triple negative breast cancer stabilizes FAK and promotes lung metastasis.Oncogene · 2026Article
- EPBAM: annotation-robust detection of alternative splicing events and a systematic benchmarking of current tools.Briefings in bioinformatics · 2026Article
- EP300-Mediated MTF1-K218 Lactylation Buffers AR-Driven Copper Overload to Suppress Cuproptosis in Castration-Resistant Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ADT and activation of HGF and WNT axes in double-null prostate cancer.Nature reviews. Urology · 2026Review
- ZRANB1 promotes cell proliferation and lymph node metastasis through SF3B3-mediated alternative splicing of CHEK2 in urothelial bladder cancer.Cell death & disease · 2026Article
- Circulating Tumor DNA as Emerging Predictive and Prognostic Biomarker in Prostate Cancer.Cancers · 2026Review
- Liquid Biopsy in Advanced Prostate Cancer.Cancers · 2026Review
- Splicing factor TRA2B enhances synthesis of androgen receptor variant AR-V7 in prostate cancer cells.The Journal of clinical investigation · 2026Article
- Androgen receptor splice variant 7 expression levels distinguish AR-mutated from nonmutated metastatic castration-resistant prostate cancers.The Journal of clinical investigation · 2026Article
- Unraveling the intricacies of small cell lung cancer: FAK splicing variants as a new feature and therapeutic vulnerability of small cell lung cancer.MedScience · 2026Article
- Identification and In Silico Characterization of an Alternatively Spliced Novel Transcript of Human DDR2 Gene.Cell biochemistry and biophysics · 2026Article
- Inhibition of nuclear import suppresses androgen receptor action and overcomes resistance in prostate cancer.BMC cancer · 2026Article
- Emerging therapies to overcome antiandrogen resistance and beyond in lethal prostate cancer.Journal of the National Cancer Center · 2026Review
- Prostate Cancer: Etiology, Diagnosis, and Treatment.Serican journal of medicine · 2026Article
- TRPML1 inhibitor ML-SI1 suppresses prostate cancer through dual regulation of androgen receptor and polyamine metabolism.Frontiers in medicine · 2026Article
- Androgen receptor splice variant expression and prostate cancer recurrence after salvage therapy.NPJ precision oncology · 2025Article
- Rewiring the transcriptome: diagnostic and therapeutic implications of alternative splicing in solid cancers.Molecular biology reports · 2025Review
63 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Androgen receptor (AR) splice variants (AR-Vs) have been implicated in the development and progression of metastatic prostate cancer. AR-Vs are truncated isoforms of the AR, a subset of which lack a ligand-binding domain and remain constitutively active in the absence of circulating androgens, thus promoting cancer cell proliferation. Consequently, AR-Vs have been proposed to contribute not only to resistance to anti-androgen therapies but also to resistance to radiotherapy in patients receiving combination therapy by promoting DNA repair. AR-Vs, such as AR-V7, have been associated with unfavourable clinical outcomes in patients; however, attempts to specifically inhibit or prevent the formation of AR-Vs have, to date, been unsuccessful. Thus, novel therapeutic strategies are desperately needed to address the oncogenic effects of AR-Vs, which can drive lethal forms of prostate cancer. Disruption of alternative splicing through modulation of the spliceosome is one such potential therapeutic avenue; however, our understanding of the biology of the spliceosome and how it contributes to prostate cancer remains incomplete, as reflected in the dearth of spliceosome-targeted therapeutic agents. In this Review, the authors outline the current understanding of the role of the spliceosome in the progression of prostate cancer and explore the therapeutic utility of manipulating alternative splicing to improve patient care.
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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.