ArticleInternational journal of cancer2013
Methylselenol prodrug enhances MDV3100 efficacy for treatment of castration-resistant prostate cancer.
Article in International journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Selenium compounds for cancer prevention and therapy - human clinical trial considerations.Medical review (2021) · 2025Review
- Targeting INMT and interrupting its methylation pathway for the treatment of castration resistant prostate cancer.Journal of experimental & clinical cancer research : CR · 2021Article
- Toxicology and pharmacology of synthetic organoselenium compounds: an update.Archives of toxicology · 2021Review
- Mithramycin suppresses DNA damage repair via targeting androgen receptor in prostate cancer.Cancer letters · 2020Article
- Raddeanin A down-regulates androgen receptor and its splice variants in prostate cancer.Journal of cellular and molecular medicine · 2019Article
- Role of GDF15 in methylseleninic acid-mediated inhibition of cell proliferation and induction of apoptosis in prostate cancer cells.PloS one · 2019Article
- Strategy for Tumor-Selective Disruption of Androgen Receptor Function in the Spectrum of Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018Article
- Interplay between Cytoplasmic and Nuclear Androgen Receptor Splice Variants Mediates Castration Resistance.Molecular cancer research : MCR · 2017Article
- Molecular Mechanisms of Enzalutamide Resistance in Prostate Cancer.Current molecular biology reports · 2017Review
- Emerging data on androgen receptor splice variants in prostate cancer.Endocrine-related cancer · 2016Review
- Androgen Receptor Splice Variants Dimerize to Transactivate Target Genes.Cancer research · 2015Article
- Methylselenocysteine preventing castration-resistant progression of prostate cancer.The Prostate · 2015Article
- Article
- Overview on the complexity of androgen receptor-targeted therapy for prostate cancer.Cancer cell international · 2015Article
- Niclosamide inhibits androgen receptor variants expression and overcomes enzalutamide resistance in castration-resistant prostate cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Androgen receptor splice variants activating the full-length receptor in mediating resistance to androgen-directed therapy.Oncotarget · 2014Article
- 20(S)-protopanaxadiol inhibition of progression and growth of castration-resistant prostate cancer.PloS one · 2014Article
- Splicing variants of androgen receptor in prostate cancer.American journal of clinical and experimental urology · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
The next-generation antiandrogen MDV3100 prolongs overall survival of patients with metastatic castration-resistant prostate cancer (CRPC). However, patient responses are variable, and survival benefit remains relatively small. Developing effective modality to improve MDV3100 efficacy is urgently needed. Recent evidence suggests that constitutively active androgen receptor splice variants (AR-Vs) drive resistance to MDV3100. In our study, we show that methylselenol prodrug downregulates the expression and activity of both the full-length AR (AR-FL) and AR-Vs. The downregulation is independent of androgen and could be attributable to repressed transcription of the AR gene. Cotreatment with methylselenol prodrug and MDV3100 suppresses AR signaling more dramatically than either agent alone, and synergistically inhibits the growth of CRPC cells in vitro. The combinatorial efficacy is observed in not only AR-V-expressing cells but also cells expressing predominantly AR-FL, likely owing to the ability of the two drugs to block the AR signaling cascade at distinct steps. Ectopic expression of AR-FL or AR-V7 attenuates the combinatorial efficacy, indicating that downregulating AR-FL and AR-V7 is importantly involved in mediating the combinatorial efficacy. Significantly, methylselenol prodrug also downregulates AR-FL and AR-Vs in vivo and substantially improves the antitumor efficacy of MDV3100. These findings support a potential combination therapy for improving MDV3100 efficacy, and provide a rationale for evaluating the clinical application of combining methylselenol prodrug with MDV3100 for the treatment of CRPC.
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What OpenQuestion holds
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.