ReviewOncotarget2016
Molecular mechanisms underlying resistance to androgen deprivation therapy in prostate cancer.
Review in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
106 citing papers in PubMed, 2 syntheses or guidelines pooled it, 163 citations in OpenAlex.
- Germacrone: A Multi-targeting Sesquiterpene with Promising Anti-cancer and Chronic Disease Applications.Anti-cancer agents in medicinal chemistry · 2024Pooled it
- Expression of microRNA-99a-3p in Prostate Cancer Based on Bioinformatics Data and Meta-Analysis of a Literature Review of 965 Cases.Medical science monitor : international medical journal of experimental and clinical research · 2018Pooled it
- Single-cell and spatial RNA sequencing in prostate cancer.Nature reviews. Urology · 2026Review
- Asymmetric cross-reactivity of nuclear receptors reveals an evolutionary buffer between estrogen and androgen signaling.iScience · 2026Article
- Testosterone and cancers: biological functions, molecular mechanisms and therapy.Molecular cancer · 2026Review
- LMNB2 promotes prostate cancer progression and epithelial-mesenchymal transition via the Wnt/β-catenin pathway.Discover oncology · 2026Article
- Anabolic-Androgenic Steroids Revisited: Structural Biology, Receptor Signaling, and Mechanisms of Anabolic-Androgenic Dissociation.International journal of molecular sciences · 2026Review
- Liposomal Delivery Systems for Improved Delivery of Docetaxel Against Prostate Cancer.International journal of nanomedicine · 2026Review
- Targeting Prostate Cancer Cells Using Anti-Sortilin and Anti-Syndecan-1 Antibody Drug Conjugates.International journal of molecular sciences · 2025Article
- Association of Germline Single Nucleotide Polymorphisms in Steroid Hormone Metabolism Pathway With Androgen Deprivation Therapy Prognosis of Prostate Cancer in Chinese Population.Cancer medicine · 2025Article
- Review
- Cancer‑associated fibroblasts in human malignancies, with a particular emphasis on sarcomas (Review).International journal of oncology · 2025Review
- Article
- Preclinical development and clinical safety assessment of a synthetic peptide conjugate enabling endogenous antibody binding to promote innate receptor engagement.Molecular therapy. Oncology · 2025Article
- Targeting PCNA/AR interaction inhibits AR-mediated signaling in castration resistant prostate cancer cells.Oncotarget · 2025Article
- Review
- PROTAC technology for prostate cancer treatment.Acta materia medica · 2025Article
- Combined Transcriptomic and Epitranscriptomic Profiling Identifies THBS1 as A Regulator of Enzalutamide Resistance in Prostate Cancer.Cancer heterogeneity and plasticity · 2025Article
- Integrative single-cell and machine learning analysis predicts lactylation-driven therapy resistance in prostate cancer: a molecular docking and experiments-validated framework for treatment optimization.Frontiers in immunology · 2025Article
- Selective killing of castration-resistant prostate cancer cells by formycin A via the ATF4-CHOP axis.Cancer science · 2024Article
46 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Prostate cancer (PCa) is the most widely diagnosed male cancer in the Western World and while low- and intermediate-risk PCa patients have a variety of treatment options, metastatic patients are limited to androgen deprivation therapy (ADT). This treatment paradigm has been in place for 75 years due to the unique role of androgens in promoting growth of prostatic epithelial cells via the transcription factor androgen receptor (AR) and downstream signaling pathways. Within 2 to 3 years of ADT, disease recurs-at which time, patients are considered to have castration-recurrent PCa (CR-PCa). A universal mechanism by which PCa becomes resistant to ADT has yet to be discovered. In this review article, we discuss underlying molecular mechanisms by which PCa evades ADT. Several major resistance pathways center on androgen signaling, including intratumoral and adrenal androgen production, AR-overexpression and amplification, expression of AR mutants, and constitutively-active AR splice variants. Other ADT resistance mechanisms, including activation of glucocorticoid receptor and impairment of DNA repair pathways are also discussed. New therapies have been approved for treatment of CR-PCa, but increase median survival by only 2-8 months. We discuss possible mechanisms of resistance to these new ADT agents. Finally, the practicality of the application of "precision oncology" to this continuing challenge of therapy resistance in metastatic or CR-PCa is examined. Empirical validation and clinical-based evidence are definitely needed to prove the superiority of "precision" treatment in providing a more targeted approach and curative therapies over the existing practices that are based on biological "cause-and-effect" relationship.
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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.