ReviewNature reviews. Urology2013
Adaptation or selection--mechanisms of castration-resistant prostate cancer.
Review in Nature reviews. Urology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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
71 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Addition of New Androgen Receptor Pathway Inhibitors to Docetaxel and Androgen Deprivation Therapy in Metastatic Hormone-Sensitive Prostate Cancer: A Systematic Review and Metanalysis.Current oncology (Toronto, Ont.) · 2022Pooled it
- Daidzein-engineered high-accumulation self-therapeutic nanoplatform drives androgen receptor degradation via ubiquitination-proteasome system to overcome enzalutamide resistance in castration-resistant prostate cancer.Materials today. Bio · 2026Article
- Therapeutic pressure drives the evolution of a protective ecotype characterized by AR-loss-induced senescence in prostate cancer.Theranostics · 2026Article
- FUT8 Is a Critical Driver of Prostate Tumour Growth and Can Be Targeted Using Fucosylation Inhibitors.Cancer medicine · 2025Article
- Fatty acid metabolism related gene MECR contributes to the progression of prostate cancer.Cancer cell international · 2025Article
- A Hierarchy of Luminal Transcription Factors Defines AR Cistrome and Is Lost in Neuroendocrine Prostate Cancer.Cancer heterogeneity and plasticity · 2025Article
- Development of an orally bioavailable CDK12/13 degrader and induction of synthetic lethality with AKT pathway inhibition.Cell reports. Medicine · 2024Article
- Epigenetic roles of KDM3B and KDM3C in tumorigenesis and their therapeutic implications.Cell death & disease · 2024Review
- Endoplasmic reticulum stress-related genes as prognostic and immunogenic biomarkers in prostate cancer.European journal of medical research · 2024Article
- MiR26a reverses enzalutamide resistance in a bone-tumor targeted system with an enhanced effect on bone metastatic CRPC.Journal of nanobiotechnology · 2024Article
- Exploring the resistance mechanism of triple-negative breast cancer to paclitaxel through the scRNA-seq analysis.PloS one · 2024Article
- Master Transcription Factor Reprogramming Unleashes Selective Translation Promoting Castration Resistance and Immune Evasion in Lethal Prostate Cancer.Cancer discovery · 2023Article
- Rbf/E2F1 control growth and endoreplication via steroid-independent Ecdysone Receptor signalling in Drosophila prostate-like secondary cells.PLoS genetics · 2023Article
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- Article
- ROLE OF ANDROGEN RECEPTOR-TARGETED AGENTS IN LOCALIZED PROSTATE CANCER.Acta clinica Croatica · 2022Review
- Spatio-temporal analysis of prostate tumors in situ suggests pre-existence of treatment-resistant clones.Nature communications · 2022Article
- Drug-Induced Epigenomic Plasticity Reprograms Circadian Rhythm Regulation to Drive Prostate Cancer toward Androgen Independence.Cancer discovery · 2022Article
- SLC26A4 correlates with homologous recombination deficiency and patient prognosis in prostate cancer.Journal of translational medicine · 2022Article
- Endothelial nitric oxide synthase (eNOS)-NO signaling axis functions to promote the growth of prostate cancer stem-like cells.Stem cell research & therapy · 2022Article
11 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.
Funding
Abstract
Men with advanced prostate cancer are typically treated with hormonal therapy, which leads to tumour shrinkage. However, tumours relapse and develop into the lethal form of the disease, termed castration-resistant prostate cancer (CRPC). Two distinct, but not mutually exclusive, models have been proposed in the literature to describe the onset of CRPC: adaptation and selection. Although some studies indicate that tumour cells acquire new alterations that enable them to survive in the castrated state (adaptation), other research points to the outgrowth of rare, pre-existing cells capable of surviving hormonal therapy (selection). Targeting the cells that survive hormonal therapy--by either adaptation or selection--is necessary to prevent the development of CRPC. Current research is focused on not only understanding the cellular mechanisms of CRPC, but also defining critical pathways that can be targeted with combinatorial therapies in castration-resistant cancer cells.
Indexed as
Identifiers
23247694What 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.