ReviewEndocrinology2013
Mechanisms of androgen receptor activation in castration-resistant prostate cancer.
Review in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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
58 citing papers in PubMed, 92 citations in OpenAlex.
- 3beta-HSD1-mediated steroid back-conversion maintains androgen signaling in prostate cancer.Molecular cancer research : MCR · 2026Article
- Steroid 5α-reductases in the brain: From neurosteroidogenesis to therapeutic implications.Frontiers in neuroendocrinology · 2026Review
- Quercetin Inhibits AKT Ser473 Phosphorylation and Disrupts AKT-Androgen Receptor Signaling in Castration-Resistant Prostate Cancer Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Androgen metabolism in prostate cancer: recent advances.Endocrinology · 2026Review
- The interconnection between androgen receptor and DNA damage response pathways in prostate cancer.Current urology · 2025Review
- Prostate cancer exploits BRD9-driven metabolic reprogramming to shape the aggressive phenotype.Cell death & disease · 2025Article
- Human Cytochrome P450 Cancer-Related Metabolic Activities and Gene Polymorphisms: A Review.Cells · 2024Review
- Reciprocal regulation between RACGAP1 and AR contributes to endocrine therapy resistance in prostate cancer.Cell communication and signaling : CCS · 2024Article
- Evaluation of AR, AR-V7, and p160 family as biomarkers for prostate cancer: insights into the clinical significance and disease progression.Journal of cancer research and clinical oncology · 2024Article
- MDM2 regulates the stability of AR, AR-V7, and TM4SF3 proteins in prostate cancer.Endocrine oncology (Bristol, England) · 2024Article
- Targeting sex steroid biosynthesis for breast and prostate cancer therapy.Nature reviews. Cancer · 2023Review
- Targeting PHB1 to inhibit castration-resistant prostate cancer progression in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2023Article
- Adrenal Steroids and Resistance to Hormonal Blockade of Prostate and Breast Cancer.Endocrinology · 2023Review
- Ser815 Phosphorylation stabilizes the androgen receptor homodimer and stimulates ER-stress induced cell death.Biochemical and biophysical research communications · 2023Article
- The epigenetic function of androgen receptor in prostate cancer progression.Frontiers in cell and developmental biology · 2023Review
- JAG1 Intracellular Domain Enhances AR Expression and Signaling and Promotes Stem-like Properties in Prostate Cancer Cells.Cancers · 2022Article
- Review
- Resistance to Antiandrogens in Prostate Cancer: Is It Inevitable, Intrinsic or Induced?Cancers · 2021Review
- Profiling of Androgen-Dependent Enhancer RNAs Expression in Human Prostate Tumors: Search for Malignancy Transition Markers.Research and reports in urology · 2021Article
- Natural Product-Based Studies for the Management of Castration-Resistant Prostate Cancer: Computational to Clinical Studies.Frontiers in pharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Systemic treatment of advanced prostate cancer is initiated with androgen deprivation therapy by gonadal testosterone depletion. Response durations are variable and tumors nearly always become resistant as castration-resistant prostate cancer (CRPC), which is driven, at least in part, by a continued dependence on the androgen receptor (AR). The proposed mechanisms that underlie AR function in this clinical setting are quite varied. These include intratumoral synthesis of androgens from inactive precursors, increased AR expression, AR activation through tyrosine kinase-dependent signaling, alterations in steroid receptor coactivators, and expression of a truncated AR with constitutive activity. Various pharmacologic interventions have clinically validated some of these mechanisms, such as those that require the AR ligand-binding domain. Clinical studies have failed to validate other mechanisms, and additional mechanisms have yet to be tested in patients with CRPC. Here, we review the mechanisms that elicit AR activity in CRPC, with a particular focus on recent developments.
Indexed as
Identifiers
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.