ReviewNuclear receptor signaling2008
AR, the cell cycle, and prostate cancer.
Review in Nuclear receptor signaling, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 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
189 citing papers in PubMed, 329 citations in OpenAlex.
- A Signal-Finding Study of Abemaciclib in Heavily Pretreated Patients with Metastatic Castration-Resistant Prostate Cancer: Results from CYCLONE 1.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Trial
- Jaboticaba peel extract limits castration-resistant prostate cancer aggressiveness by counteracting EMT through steroid hormone and TGF-β signaling modulation.Journal of molecular histology · 2026Article
- Single-threshold-guided adaptive cancer therapy with partial-cycle treatment: A mechanistic and reinforcement learning analysis.PLoS computational biology · 2026Article
- Androgen receptor contributes to radioresistance through DNA repair and autophagy in AR-positive prostate cancer cells.bioRxiv : the preprint server for biology · 2025Article
- The landscape of cyclin-dependent kinase 4/6 inhibitors in solid malignancies: emphasis on immunotherapy combinatorial strategies.Medical oncology (Northwood, London, England) · 2025Review
- Fatty acid binding protein 5 inhibitors as novel anticancer agents against metastatic castration-resistant prostate cancer.Bioorganic & medicinal chemistry · 2025Article
- Triplet therapy for metastatic castration-sensitive prostate cancer: Rationale and clinical evidence.International journal of urology : official journal of the Japanese Urological Association · 2025Review
- Post-eclosion growth in the Drosophila ejaculatory duct is driven by Juvenile hormone signaling and is essential for male fertility.Developmental biology · 2025Article
- Review
- Androgen Receptor Expression Governs the Seasonal Inhibition of Testicular Development and Subsequent Recovery inBiology · 2025Article
- Discovery of Essential Genes as Possible Targets for Prostate Cancer Drug Development.International journal of genomics · 2025Article
- A Hierarchy of Luminal Transcription Factors Defines AR Cistrome and Is Lost in Neuroendocrine Prostate Cancer.Cancer heterogeneity and plasticity · 2025Article
- Unveiling the Potential of S4 on Non-small Cell Lung Cancer Cells: Impact on Proliferation, Apoptosis, Senescence, and Metabolome Profile.Anti-cancer agents in medicinal chemistry · 2025Article
- Interactions between key genes and pathways in prostate cancer progression and therapy resistance.Frontiers in oncology · 2025Review
- Article
- Post-eclosion growth in thebioRxiv : the preprint server for biology · 2024Article
- AR coactivators, CBP/p300, are critical mediators of DNA repair in prostate cancer.bioRxiv : the preprint server for biology · 2024Article
- The Evolving Pathways of the Efficacy of and Resistance to CDK4/6 Inhibitors in Breast Cancer.Cancers · 2023Review
- Impact of FKBP52 on cell proliferation and hormone-dependent cancers.Cancer science · 2023Review
- Prohibitin Links Cell Cycle, Motility and Invasion in Prostate Cancer Cells.International journal of molecular sciences · 2023Article
129 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 2 institutions in 1 country.
Funding
Abstract
The androgen receptor (AR) is a critical effector of prostate cancer development and progression. The dependence of this tumor type on AR activity is exploited in treatment of disseminated prostate cancers, wherein ablation of AR function (achieved either through ligand depletion and/or the use of AR antagonists) is the first line of therapeutic intervention. These strategies are initially effective, and induce a mixed response of cell cycle arrest or apoptosis in prostate cancer cells. However, recurrent, incurable tumors ultimately arise as a result of inappropriately restored AR function. Based on these observations, it is imperative to define the mechanisms by which AR controls cancer cell proliferation. Mechanistic investigation has revealed that AR acts as a master regulator of G1-S phase progression, able to induce signals that promote G1 cyclin-dependent kinase (CDK) activity, induce phosphorylation/inactivation of the retinoblastoma tumor suppressor (RB), and thereby govern androgen-dependent proliferation. These functions appear to be independent of the recently identified TMPRSS2-ETS fusions. Once engaged, several components of the cell cycle machinery actively modulate AR activity throughout the cell cycle, thus indicating that crosstalk between the AR and cell cycle pathways likely modulate the mitogenic response to androgen. As will be discussed, discrete aberrations in this process can alter the proliferative response to androgen, and potentially subvert hormonal control of tumor progression.
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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.