Evidence map›Paper›PMID 21705451›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2011

Potential prostate cancer drug target: bioactivation of androstanediol by conversion to dihydrotestosterone.

James L Mohler, Mark A Titus, Elizabeth M Wilson

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

36 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. 5α-reductase type 1 modulates insulin sensitivity in men.The Journal of clinical endocrinology and metabolism · 2014
    Trial
  5. Article
  6. Review
  7. Article
  8. Article
  9. Hijacking Sexual Immuno-Privilege in GBM-An Immuno-Evasion Strategy.International journal of molecular sciences · 2021
    Article
  10. Article
  11. Pictet-Spengler condensations using 4-(2-aminoethyl)coumarins.New journal of chemistry = Nouveau journal de chimie · 2020
    Article
  12. Article
  13. Intracrinology-revisited and prostate cancer.The Journal of steroid biochemistry and molecular biology · 2020
    Review
  14. Review
  15. Article
  16. Dehydroepiandrosterone (DHEA)-SOVitamins and hormones · 2018
    Review
  17. Aldo-Keto Reductase (AKR) 1C3 inhibitors: a patent review.Expert opinion on therapeutic patents · 2017
    Review
  18. Review
  19. Article
  20. Review
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

3 authors at 2 institutions in 1 country.

James L MohlerDepartment of Urology, Roswell Park Cancer Institute, Department of Urology, University at Buffalo, State University of New York, Buffalo, New York, USA.
Mark A Titus
Elizabeth M Wilson
University at Buffalo, State University of New York · USRoswell Park Comprehensive Cancer Center · US

Funding

Tumor stem cells in androgen independent prostate cancerP01CA077739 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MOHLER, JAMES L · 1998 to 2014
$16.8M
ANDROGEN RECEPTOR REGULATION OF REPRODUCTIVE FUNCTIONR01HD016910 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI WILSON, ELIZABETH M. · 1985 to 2010
$2.8M
ANDROGEN RECEPTOR REGULATION OF REPRODUCTIVE FUNCTIONR37HD016910 · NICHD · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI WILSON, ELIZABETH M. · 1993 to 2002
$1.1M
NCI NIH HHS CA16156NCI NIH HHS CA34026NCI NIH HHS P01 CA077739NCI NIH HHS P01-CA77739NCI NIH HHS PC094304NICHD NIH HHS HD16910NICHD NIH HHS R01 HD016910NICHD NIH HHS R37 HD016910
6 · The paper itself

Abstract

High-affinity binding of dihydrotestosterone (DHT) to the androgen receptor (AR) initiates androgen-dependent gene activation, required for normal male sex development in utero, and contributes to prostate cancer development and progression in men. Under normal physiologic conditions, DHT is synthesized predominantly by 5α-reduction of testosterone, the major circulating androgen produced by the testis. During androgen deprivation therapy, intratumoral androgen production is sufficient for AR activation and prostate cancer growth, even though circulating testicular androgen levels are low. Recent studies indicate that the metabolism of 5α-androstane-3α, 17β-diol by 17β-hydroxysteroid dehydrogenase 6 in benign prostate and prostate cancer cells is a major biosynthetic pathway for intratumoral synthesis of DHT, which binds AR and initiates transactivation to promote prostate cancer growth during androgen deprivation therapy. Drugs that target the so-called backdoor pathway of DHT synthesis provide an opportunity to enhance clinical response to luteinizing-hormone-releasing hormone (LHRH) agonists or antagonists, AR antagonists, and inhibitors of 5α-reductase enzymes (finasteride or dutasteride), and other steroid metabolism enzyme inhibitors (ketoconazole or the recently available abiraterone acetate).

Indexed as

AndrostenediolCholestenone 5 alpha-ReductaseDihydrotestosteroneEnzyme InhibitorsHumansMaleMolecular Targeted TherapyProstatic NeoplasmsSignal TransductionSteroid 17-alpha-HydroxylaseAndrostenediolCholestenone 5 alpha-ReductaseCYP17A1 protein, humanDihydrotestosteroneEnzyme InhibitorsSteroid 17-alpha-Hydroxylase

Identifiers

PMID21705451
PMCPMC3177006
OpenAlexW2132986013

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.