ArticleCurrent genomics2009
The role of androgen receptor mutations in prostate cancer progression.
Article in Current genomics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 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
87 citing papers in PubMed, 179 citations in OpenAlex.
- The prognostic significance of combined ERG and androgen receptor expression in patients with prostate cancer managed by androgen deprivation therapy.Cancer biology & therapy · 2014Trial
- From prostate specific antigen to genomic signatures: Advances in biomarkers for prostate cancer diagnosis and prognosis.Translational oncology · 2026Review
- Disruption of androgen receptor-cofactor interactions by the RNA-binding protein FUS/TLS alters androgen signalling in prostate cancer.Oncogene · 2026Article
- Circulating tumour DNA in mCRPC: bridging tumour biology and real-time treatment monitoring.Frontiers in molecular medicine · 2026Review
- Androgen receptor reactivation in castration-resistant prostate cancer: mechanisms, epigenetic adaptation, and therapeutic vulnerabilities.Frontiers in oncology · 2026Review
- The molecular aspects in prostatic cancer, unraveling the role of CDKs in prostate cancer progression.Discover oncology · 2025Review
- Current Role and Future Frontiers of Spatial Transcriptomics in Genitourinary Cancers.Cancers · 2025Review
- Targeting androgen receptor stability and degradation: approaches for developing a therapy for spinal and bulbar muscular atrophy.Cell communication and signaling : CCS · 2025Review
- Androgen Receptor Signalling in Prostate Cancer: Mechanisms of Resistance to Endocrine Therapies.Research and reports in urology · 2025Review
- Thieno[2,3-Endocrine oncology (Bristol, England) · 2025Article
- PARP-ish: Gaps in Molecular Understanding and Clinical Trials Targeting PARP Exacerbate Racial Disparities in Prostate Cancer.Cancer research · 2024Review
- Enhanced eMAGE applied to identify genetic factors of nuclear hormone receptor dysfunction via combinatorial gene editing.Nature communications · 2024Article
- Insight into Recent Advances in Degrading Androgen Receptor for Castration-Resistant Prostate Cancer.Cancers · 2024Review
- AR activates YAP/TAZ differentially in prostate cancer.Life science alliance · 2023Article
- Whole-exome sequencing of Indian prostate cancer reveals a novel therapeutic target: POLQ.Journal of cancer research and clinical oncology · 2023Article
- Review
- Multi-institutional Analysis of the Clinical and Genomic Characteristics of Black Patients with Metastatic Hormone-Sensitive Prostate Cancer.The oncologist · 2022Article
- H3K27ac HiChIP in prostate cell lines identifies risk genes for prostate cancer susceptibility.American journal of human genetics · 2021Article
- Review
- Targeting the Lnc-OPHN1-5/androgen receptor/hnRNPA1 complex increases Enzalutamide sensitivity to better suppress prostate cancer progression.Cell death & disease · 2021Article
27 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
No grant is acknowledged in the PubMed record.
Abstract
Prostate tumour growth is almost always dependent upon the androgen receptor pathway and hence therapies aimed at blocking this signalling axis are useful tools in the management of this disease. Unfortunately such therapies invariably fail; and the tumour progresses to an "androgen-independent" stage. In such cases androgen receptor expression is almost always maintained and much evidence exists to suggest that it may still be driving growth. One mechanism by which the receptor is thought to remain active is mutation. This review summarises the present data on androgen receptor mutations in prostate cancer, and how such substitutions offer a growth advantage by affecting cofactor interactions or by reducing ligand specificity. Such alterations appear to have a subsequent effect upon gene expression suggesting that tumours may "behave" differently dependent upon the ligand promoting growth and if a mutation is present.
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.