Evidence map›Paper›PMID 21689727›Full record

ReviewMolecular and cellular endocrinology2012

Androgen receptor gene polymorphisms and alterations in prostate cancer: of humanized mice and men.

Diane M Robins

Open access · greenAbstract readReview
In one paragraph

Review in Molecular and cellular endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 19% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Prostate cancer.Nature reviews. Disease primers · 2021
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Regulators of gene expression as biomarkers for prostate cancer.American journal of cancer research · 2012
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Diane M RobinsDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, MI 48109-5618, USA. drobins@umich.edu
University of Michigan–Ann Arbor · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
MICHIGAN INSTITUTE FOR CLINICAL AND HEALTH RESEARCH (MICHR) (UL1): (BPCA)UL1RR024986 · NCRR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHANLEY, THOMAS P. · 2007 to 2011
$51.2M
VACCINIA PSA FOR ANDROGEN-MODULATED POST-SURGICAL RECURRENCE OF PROSTATE CANCERP50CA069568 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI COONEY, KATHLEEN A · 1995 to 2013
$31.3M
PUBLIC HEALTH DEMONSTRATIONP60DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MYERS, MARTIN G · 1985 to 2012
$26.5M
Genetic Dissection of Context-Dependent and Opposing Roles of Androgen ReceptorR01CA144032 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROBINS, DIANE M. · 2010 to 2014
$1.5M
MECHANISM OF STEROID SPECIFIC GENE ACTIVATIONR01DK056356 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROBINS, DIANE M. · 1999 to 2003
$1.3M
NCI NIH HHS 5 P30 CA46592NCI NIH HHS P30 CA046592NCI NIH HHS P50 CA069568NCI NIH HHS P50-CA69568NCI NIH HHS R01 CA144032NCRR NIH HHS UL1 RR024986NIDDK NIH HHS 5 P60 DK20572NIDDK NIH HHS P60 DK020572NIDDK NIH HHS R01 DK056356PHS HHS R01-144032PHS HHS R01-56356
6 · The paper itself

Abstract

Germline polymorphisms and somatic mutations of the androgen receptor (AR) have been intensely investigated in prostate cancer but even with genomic approaches their impact remains controversial. To assess the functional significance of AR genetic variation, we converted the mouse gene to the human sequence by germline recombination and engineered alleles to query the role of a polymorphic glutamine (Q) tract implicated in cancer risk. In a prostate cancer model, AR Q tract length influences progression and castration response. Mutation profiling in mice provides direct evidence that somatic AR variants are selected by therapy, a finding validated in human metastases from distinct treatment groups. Mutant ARs exploit multiple mechanisms to resist hormone ablation, including alterations in ligand specificity, target gene selectivity, chaperone interaction and nuclear localization. Regardless of their frequency, these variants permute normal function to reveal novel means to target wild type AR and its key interacting partners.

Indexed as

AnimalsGenetic EngineeringHumansMaleMicePolymorphism, GeneticProstatic NeoplasmsReceptors, AndrogenReceptors, Androgen

Identifiers

PMID21689727
PMCPMC3188356
OpenAlexW1966996152

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.