Evidence map›Paper›PMID 32371590›Full record

ArticleMolecular cancer therapeutics2020

Targeting the PI3K/AKT Pathway Overcomes Enzalutamide Resistance by Inhibiting Induction of the Glucocorticoid Receptor.

Remi Adelaiye-Ogala, Berkley E Gryder, Yen Thi Minh Nguyen, Aian Neil Alilin, Adlai R Grayson, Wardah Bajwa, Keith H Jansson, Michael L Beshiri, Supreet Agarwal, Jose Antonio Rodriguez-Nieves and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cancer therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
4.4field-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

37 citing papers in PubMed, 51 citations in OpenAlex.

  1. Phase Ib/II Study of Enzalutamide with Samotolisib (LY3023414) or Placebo in Patients with Metastatic Castration-Resistant Prostate Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Trial
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  6. Observational
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  11. Metabolic and imaging phenotypes associated withbioRxiv : the preprint server for biology · 2025
    Article
  12. Review
  13. Translational andrology and urology · 2024
    Review
  14. Article
  15. Review
  16. Article
  17. Downregulated antisense lncRNAAmerican journal of cancer research · 2024
    Article
  18. Targeting PI3K/Akt signaling in prostate cancer therapy.Journal of cell communication and signaling · 2023
    Review
  19. Article
  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

13 authors at 3 institutions in 1 country.

Remi Adelaiye-OgalaLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.ORCID 0000-0002-6581-7359
Berkley E GryderOncogenomics Section, Genetics Branch, NCI, NIH, Bethesda, Maryland.ORCID 0000-0003-0130-2302
Yen Thi Minh NguyenLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Aian Neil AlilinLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Adlai R GraysonLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Wardah BajwaLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Keith H JanssonLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Michael L BeshiriLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Supreet AgarwalLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Jose Antonio Rodriguez-NievesLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Brian CapaldoLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Kathleen KellyLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
David J VanderWeeleLaboratory for Genitourinary Cancer Pathogenesis, Center for Cancer Research, NCI, NIH, Bethesda, Maryland. david.vanderweele@northwestern.edu.ORCID 0000-0003-4576-5034
Center for Cancer Research · USNational Institutes of Health · USNorthwestern University · US

Funding

Mechanisms of pathogenesis in patient derived organoid models of prostate cancerZIABC011782 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KELLY, KATHLEEN · 2017 to 2024
$8.2M
Mechanisms of resistance to Androgen Receptor inhibition in prostate cancerZIABC011713 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI VANDERWEELE, DAVID · 2016 to 2018
$1.9M
Development of therapy for aggressive variant prostate cancerZIABC011771 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI VANDERWEELE, DAVID · 2017 to 2018
$79k
Evolution of prostate cancer genomeZIABC011770 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI VANDERWEELE, DAVID · 2017 to 2017
$43k
Intramural NIH HHS Z99 CA999999Intramural NIH HHS ZIA BC011713Intramural NIH HHS ZIA BC011770Intramural NIH HHS ZIA BC011771Intramural NIH HHS ZIA BC011782
6 · The paper itself

Abstract

The PI3K-AKT pathway has pleiotropic effects and its inhibition has long been of interest in the management of prostate cancer, where a compensatory increase in PI3K signaling has been reported following androgen receptor (AR) blockade. Prostate cancer cells can also bypass AR blockade through induction of other hormone receptors, in particular the glucocorticoid receptor (GR). Here we demonstrate that AKT inhibition significantly decreases cell proliferation through both cytostatic and cytotoxic effects. The cytotoxic effect is enhanced by AR inhibition and is most pronounced in models that induce compensatory GR expression. AKT inhibition increases canonical AR activity and remodels the chromatin landscape, decreasing enhancer interaction at the GR gene (

Indexed as

AnimalsApoptosisBenzamidesCell ProliferationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMaleMiceNitrilesPhenylthiohydantoinPhosphatidylinositol 3-KinasesPiperazinesProstatic NeoplasmsProto-Oncogene Proteins c-aktPyrimidinesAR protein, humanBenzamidesenzalutamideipatasertibNitrilesPhenylthiohydantoinPhosphatidylinositol 3-KinasesPiperazinesProto-Oncogene Proteins c-aktPyrimidinesReceptors, AndrogenReceptors, Glucocorticoid

Identifiers

PMID32371590
PMCPMC8522555
OpenAlexW3023616492

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.