Evidence map›Paper›PMID 23813697›Full record

ArticleThe Prostate2013

Prostate cancer cells differ in testosterone accumulation, dihydrotestosterone conversion, and androgen receptor signaling response to steroid 5α-reductase inhibitors.

Yue Wu, Alejandro Godoy, Faris Azzouni, John H Wilton, Clement Ip, James L Mohler

Abstract read
In one paragraph

Article in The Prostate, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  11. Differential Associations of SLCO Transporters with Prostate Cancer Aggressiveness between African Americans and European Americans.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2021
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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

6 authors at 1 institution in 2 countries.

Yue WuDepartment of Cancer Prevention and Control, Roswell Park Cancer Institute, Buffalo, New York 14263, USA.
Alejandro Godoy
Faris Azzouni
John H Wilton
Clement Ip
James L Mohler
Roswell Park Comprehensive Cancer Center · US

Funding

Two-Spirit Films in Indigenous Cancer HealthP30CA016056 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI Dean G. Tang · 1985 to 2026
$116.6M
Tumor stem cells in androgen independent prostate cancerP01CA077739 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MOHLER, JAMES L · 1998 to 2014
$16.8M
Translational Research of Finasteride and Selenium Prevention of Prostate CancerP01CA126804 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI IP, CLEMENT C · 2007 to 2011
$5.3M
NCI NIH HHS P01 CA077739NCI NIH HHS P01 CA126804NCI NIH HHS P01CA126804NCI NIH HHS P01CA77739NCI NIH HHS P30 CA016056NCI NIH HHS P30CA16056
6 · The paper itself

Abstract

backgroundBlocking 5α-reductase-mediated testosterone conversion to dihydrotestosterone (DHT) with finasteride or dutasteride is the driving hypothesis behind two prostate cancer prevention trials. Factors affecting intracellular androgen levels and the androgen receptor (AR) signaling axis need to be examined systematically in order to fully understand the outcome of interventions using these drugs.

methodsThe expression of three 5α-reductase isozymes, as determined by immunohistochemistry and qRT-PCR, was studied in five human prostate cancer cell lines. Intracellular testosterone and DHT were analyzed using mass spectrometry. A luciferase reporter assay and AR-regulated genes were used to evaluate the modulation of AR activity.

resultsProstate cancer cells were capable of accumulating testosterone to a level 15-50 times higher than that in the medium. The profile and expression of 5α-reductase isozymes did not predict the capacity to convert testosterone to DHT. Finasteride and dutasteride were able to depress testosterone uptake in addition to lowering intracellular DHT. The inhibition of AR activity following drug treatment often exceeded the expected response due to reduced availability of DHT. The ability to maintain high intracellular testosterone might compensate for the shortage of DHT.

conclusionsThe biological effect of finasteride or dutasteride appears to be complex and may depend on the interplay of several factors, which include testosterone turnover, enzymology of DHT production, ability to use testosterone and DHT interchangeably, and propensity of cells for off-target AR inhibitory effect.

Indexed as

5-alpha Reductase InhibitorsAzasteroidsCell Line, TumorDihydrotestosteroneDutasterideFinasterideHumansMaleProstateProstatic NeoplasmsReceptors, AndrogenSignal TransductionTandem Mass SpectrometryTestosterone5-alpha Reductase InhibitorsAzasteroidsDihydrotestosteroneDutasterideFinasterideReceptors, AndrogenTestosteroneandrogen receptordihydrotestosteronedutasteridefinasterideprostate cancersteroid 5α-reductasetestosterone

Identifiers

PMID23813697
PMCPMC3999702
OpenAlexW2166514285

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.