Evidence map›Paper›PMID 31271415›Full record

ReviewEndocrinology2019

HSD3B1 Genotypes Conferring Adrenal-Restrictive and Adrenal-Permissive Phenotypes in Prostate Cancer and Beyond.

Navin Sabharwal, Nima Sharifi

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.6field-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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Proceedings of the National Academy of Sciences of the United States of America · 2020
    Trial
  4. Article
  5. Serendipity, steroids and science.The Journal of steroid biochemistry and molecular biology · 2026
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. BMX controls 3βHSD1 and sex steroid biosynthesis in cancer.The Journal of clinical investigation · 2023
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  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

2 authors at 2 institutions in 1 country.

Navin SabharwalGenitourinary Malignancies Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Nima SharifiGenitourinary Malignancies Research Center, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.
Cleveland Clinic · USCleveland Clinic Lerner College of Medicine · US

Funding

Elucidating a novel molecular biomarker for castration-resistant prostate cancerR01CA172382 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Nima Sharifi · 2012 to 2026
$5.2M
Compensatory steroidogenesis mechanisms in castration-resistant prostate cancerR01CA190289 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI SHARIFI, NIMA · 2015 to 2019
$2.1M
Cooperative steroidogenic inhibition for treatment of advanced prostate cancerR01CA168899 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI SHARIFI, NIMA · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA168899NCI NIH HHS R01 CA172382NCI NIH HHS R01 CA190289
6 · The paper itself

Abstract

Castration-resistant prostate cancer (PCa) almost invariably occurs after androgen deprivation therapy for metastatic disease and is driven in part by androgen synthesis within the tumor. 3β-hydroxysteroid dehydrogenase isoenzyme-1 catalyzes the conversion of adrenal precursor steroids into potent androgens essential for PCa progression. A common 1245 A→C missense-encoding single nucleotide polymorphism in HSD3B1 (rs1047303), the gene that encodes this enzyme, leads to a more stable protein that is resistant to degradation and thus increased production of potent androgens from adrenal precursors, facilitating castration-resistant PCa development. Consistent with this mechanism, this adrenal-permissive HSD3B1(1245C) genotype is associated with inferior outcomes after androgen deprivation therapy for advanced PCa, and increased sensitivity to pharmacologic blockade of adrenal precursors in metastatic disease. Herein, we review current knowledge of the mechanisms conferred by HSD3B1 genotype to alter androgen physiology and accelerate development of castration-resistant disease and its associations with clinical PCa outcomes. In light of its effect on steroid physiology, we also discuss its potential associations with non-PCa phenotypes.

Indexed as

Adrenal GlandsAndrogensDehydroepiandrosteroneDietary SupplementsGenotypeHumansMaleMultienzyme ComplexesPhenotypeProgesterone ReductaseProstatic Neoplasms, Castration-ResistantSteroid Isomerases3 beta-hydroxysteroid oxidoreductase-delta(5) 3-ketosteroid isomeraseAndrogensDehydroepiandrosteroneMultienzyme ComplexesProgesterone ReductaseSteroid Isomerases

Identifiers

PMID31271415
PMCPMC6736215
OpenAlexW2955965693

What OpenQuestion holds

Textmetadata
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.