Evidence map›Paper›PMID 24948873›Full record

ReviewInternational journal of biological sciences2014

Beyond T and DHT - novel steroid derivatives capable of wild type androgen receptor activation.

Elahe A Mostaghel

Open access · goldAbstract readReview
In one paragraph

Review in International journal of biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 44 citations in OpenAlex.

  1. Gut Bacteria Improve Depressive Symptoms by Degrading Cortisol into Androgen.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. TheJournal of lipid research · 2018
    Article
  8. Article
  9. Review
  10. Androgen Signaling in Prostate Cancer.Cold Spring Harbor perspectives in medicine · 2017
    Review
  11. The hunt for a selective 17,20 lyase inhibitor; learning lessons from nature.The Journal of steroid biochemistry and molecular biology · 2016
    Review
  12. Review
  13. Review
  14. Article
  15. 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.

Elahe A MostaghelDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle WA, USA.
Fred Hutch Cancer Center · US

Funding

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

Abstract

While androgen deprivation therapy (ADT) remains the primary treatment for metastatic prostate cancer (PCa), castration does not eliminate androgens from the prostate tumor microenvironment, and residual intratumoral androgens are implicated in nearly every mechanism by which androgen receptor (AR)-mediated signaling promotes castration-resistant disease. The uptake and intratumoral (intracrine) conversion of circulating adrenal androgens such as dehydroepiandrosterone sulfate (DHEA-S) to steroids capable of activating the wild type AR is a recognized driver of castration resistant prostate cancer (CRPC). However, less well-characterized adrenal steroids, including 11-deoxcorticosterone (DOC) and 11beta-hydroxyandrostenedione (11OH-AED) may also play a previously unrecognized role in promoting AR activation. In particular, recent data demonstrate that the 5α-reduced metabolites of DOC and 11OH-AED are activators of the wild type AR. Given the well-recognized presence of SRD5A activity in CRPC tissue, these observations suggest that in the low androgen environment of CRPC, alternative sources of 5α-reduced ligands may supplement AR activation normally mediated by the canonical 5α-reduced agonist, 5α-DHT. Herein we review the emerging data that suggests a role for these alternative steroids of adrenal origin in activating the AR, and discuss the enzymatic pathways and novel downstream metabolites mediating these effects. We conclude by discussing the potential implications of these findings for CRPC progression, particularly in context of new agents such as abiraterone and enzalutamide which target the AR-axis for prostate cancer therapy.

Indexed as

AndrogensAntineoplastic AgentsDesoxycorticosteroneHumansMaleProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantReceptors, AndrogenAndrogensAntineoplastic AgentsAR protein, humanDesoxycorticosteroneReceptors, Androgen11beta-hydroxyandrostenedione11ketodihydrotestosteroneadrenal androgenandrogen receptor.castration resistant prostate cancerdeoxycorticosteroneintracrine steroidogenesis

Identifiers

PMID24948873
PMCPMC4062953
OpenAlexW2129134066

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.