Evidence map›Paper›PMID 26797685›Full record

ReviewHormones & cancer2016

Classical and Non-Classical Roles for Pre-Receptor Control of DHT Metabolism in Prostate Cancer Progression.

Ailin Zhang, Jiawei Zhang, Stephen Plymate, Elahe A Mostaghel

Open access · greenAbstract readReview
In one paragraph

Review in Hormones & cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  19. Review
  20. Intracrine androgen biosynthesis and drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2020
    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

4 authors at 3 institutions in 2 countries.

Ailin ZhangDivision of Clinical Research, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, MS D5-380, Seattle, WA, 98109, USA.
Jiawei ZhangSchool of Medicine, Beijing University of Chinese Medicine, Beijing, 100029, China.
Stephen PlymateDepartment of Medicine, University of Washington, Seattle, WA, 98104, USA.
Elahe A MostaghelDivision of Clinical Research, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave N, MS D5-380, Seattle, WA, 98109, USA. emostagh@fhcrc.org.
Fred Hutch Cancer Center · USBeijing University of Chinese Medicine · CNUniversity of Washington · US

Funding

TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
NCI NIH HHS P50 CA097186NCI NIH HHS P50 CA97186
6 · The paper itself

Abstract

Androgens play an important role in prostate cancer (PCa) development and progression. Accordingly, androgen deprivation therapy remains the front-line treatment for locally recurrent or advanced PCa, but patients eventually relapse with the lethal form of the disease termed castration resistant PCa (CRPC). Importantly, castration does not eliminate androgens from the prostate tumor microenvironment which is characterized by elevated tissue androgens that are well within the range capable of activating the androgen receptor (AR). In this mini-review, we discuss emerging data that suggest a role for the enzymes mediating pre-receptor control of dihydrotestosterone (DHT) metabolism, including AKR1C2, HSD17B6, HSD17B10, and the UGT family members UGT2B15 and UGT2B17, in controlling intratumoral androgen levels, and thereby influencing PCa progression. We review the expression of steroidogenic enzymes involved in this pathway in primary PCa and CRPC, the activity and regulation of these enzymes in PCa experimental models, and the impact of genetic variation in genes mediating pre-receptor DHT metabolism on PCa risk. Finally, we discuss recent data that suggests several of these enzymes may also play an unrecognized role in CRPC progression separate from their role in androgen inactivation.

Indexed as

Drug Resistance, Neoplasm3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)3-Hydroxyacyl CoA DehydrogenasesAnimalsDihydrotestosteroneDisease ProgressionGene Expression Regulation, NeoplasticGlucuronosyltransferaseHumansHydroxysteroid DehydrogenasesMaleMinor Histocompatibility AntigensProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantRacemases and EpimerasesReceptors, Androgen3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)3-Hydroxyacyl CoA DehydrogenasesAKR1C2 protein, humanAR protein, humanDihydrotestosteroneGlucuronosyltransferaseHSD17B10 protein, humanHSD17B6 protein, humanHydroxysteroid DehydrogenasesMinor Histocompatibility AntigensRacemases and EpimerasesReceptors, AndrogenUDP-glucuronosyltransferase 2B15, humanUGT2B17 protein, human

Identifiers

PMID26797685
PMCPMC4859429
OpenAlexW2297660672

What OpenQuestion holds

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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.