Evidence map›Paper›PMID 23748150›Full record

ReviewThe Journal of steroid biochemistry and molecular biology2013

AKR1C3 as a target in castrate resistant prostate cancer.

Adegoke O Adeniji, Mo Chen, Trevor M Penning

Abstract readReview
In one paragraph

Review in The Journal of steroid biochemistry and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

70 citing papers in PubMed, 136 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. The structural basis of aldo-keto reductase 1C3 inhibition by 17α-picolyl and 17(Journal of enzyme inhibition and medicinal chemistry · 2025
    Article
  9. Metabolic activation of flunitrazepam via nitroreduction mediated by aldo-keto reductase 1C3.Drug metabolism and disposition: the biological fate of chemicals · 2025
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. 30th Annual GPPharmaceuticals (Basel, Switzerland) · 2023
    Article
  19. Article
  20. Article

10 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Adegoke O AdenijiDepartment of Pharmacology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6061, USA.
Mo Chen
Trevor M Penning
University of Pennsylvania · US

Funding

Translational Research Support CoreP30ES013508 · NIEHS · UNIVERSITY OF PENNSYLVANIA · PI Rebecca A Simmons · 2006 to 2026
$35.3M
Institutional Clinical and Translational Science AwardKL2RR024132 · NCRR · UNIVERSITY OF PENNSYLVANIA · PI FITZGERALD, GARRET A · 2006 to 2011
$5.1M
Human Aldo Keto Reductases and Steroid Hormone ActionR01CA090744 · NCI · UNIVERSITY OF PENNSYLVANIA · PI PENNING, TREVOR M · 2001 to 2011
$3.1M
Kinetic and structural analysis of human steroid 5beta-reductase (AKR1D1)F32DK089827 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI CHEN, MO · 2011 to 2012
$104k
NCI NIH HHS R01 CA090744NCI NIH HHS R01-CA90744NCRR NIH HHS KL2 RR024132NIDDK NIH HHS F32-DK089827NIEHS NIH HHS P30 ES013508NIEHS NIH HHS P30-ES13508
6 · The paper itself

Abstract

Aberrant androgen receptor (AR) activation is the major driver of castrate resistant prostate cancer (CRPC). CRPC is ultimately fatal and more therapeutic agents are needed to treat this disease. Compounds that target the androgen axis by inhibiting androgen biosynthesis and or AR signaling are potential candidates for use in CRPC treatment and are currently being pursued aggressively. Aldo-keto reductase 1C3 (AKR1C3) plays a pivotal role in androgen biosynthesis within the prostate. It catalyzes the 17-ketoreduction of weak androgen precursors to give testosterone and 5α-dihydrotestosterone. AKR1C3 expression and activity has been implicated in the development of CRPC, making it a rational target. Selective inhibition of AKR1C3 will be important, however, due to the presence of closely related isoforms, AKR1C1 and AKR1C2 that are also involved in androgen inactivation. We examine the evidence that supports the vital role of AKR1C3 in CRPC and recent developments in the discovery of potent and selective AKR1C3 inhibitors. This article is part of a Special Issue entitled 'CSR 2013'.

Indexed as

3-Hydroxysteroid DehydrogenasesAldo-Keto Reductase Family 1 Member C3HumansHydroxyprostaglandin DehydrogenasesMaleOrchiectomyProstatic Neoplasms3-Hydroxysteroid DehydrogenasesAKR1C3 protein, humanAldo-Keto Reductase Family 1 Member C3Hydroxyprostaglandin DehydrogenasesAndrogensNonsteroidal anti-inflammatory drugsProstaglandin F synthaseProstate cancerType 5 17β-hydroxysteroid dehydrogenase

Identifiers

PMID23748150
PMCPMC3805777
OpenAlexW2075145938

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.