Evidence map›Paper›PMID 35993978›Full record

ReviewCritical reviews in oncogenesis2022

Phenotypic Plasticity - Alternate Transcriptional Programs Driving Treatment Resistant Prostate Cancer.

Jagpreet Singh Nanda, Praveen Koganti, Graziela Perri, Leigh Ellis

Open access · bronzeAbstract readReview
In one paragraph

Review in Critical reviews in oncogenesis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  4. Review
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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

4 authors at 1 institution in 1 country.

Jagpreet Singh NandaDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048; Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA 90048.
Praveen KogantiDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048; Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA 90048.
Graziela PerriDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048; Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA 90048.
Leigh EllisDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048; Cedars-Sinai Samuel Oschin Comprehensive Cancer Institute, Los Angeles, CA 90048; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048; Center for Bioinformatics and Functional Genomics, Cedars-Sinai Medical Center, Los Angeles, CA 90048.
Cedars-Sinai Medical Center · US

Funding

Exploiting RB1 deficiency for the treatment of lethal neuroendocrine prostate cancerR01CA207757 · NCI · ROSWELL PARK CANCER INSTITUTE CORP · PI ELLIS, LEIGH, GOODRICH, DAVID W. · 2016 to 2020
$2.8M
ATR Dependency as a Novel Therapeutic Target in Lethal RB Deficient ProstateCancerR01CA252468 · NCI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI Leigh Ellis · 2020 to 2026
$1.5M
Identifying EZH2-dependent vulnerabilities in RB deficient prostate cancerR21CA257484 · NCI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI ELLIS, LEIGH · 2021 to 2022
$425k
NCI NIH HHS R01 CA207757NCI NIH HHS R01 CA252468NCI NIH HHS R21 CA257484
6 · The paper itself

Abstract

Androgen deprivation therapy (ADT) that antagonizes androgen receptor (AR) signaling has made significant increases to overall survival of prostate cancer patients. However, ADT is not curative, and patients eventually progress to castration resistant disease (CRPC). It has become evident that a subset of prostate cancers acquire ADT resistance through mechanisms independent of AR alteration or reprogramming of AR signaling. This approximately involves a quarter of prostate cancers progressing on ADT. Collectively, these tumors evolve via phenotypic plasticity and display the activation of developmental and stemness gene signatures as well as transitional programs including an epithelial-mesenchymal phenotype. Currently, no successful treatments exist for prostate cancer patients to inhibit or reverse prostate tumor progression that utilizes mechanisms of epi-plasticity. This overview will discuss epigenetic mechanisms that mediate phenotypic plasticity and the potential for targeting the epigenome to create a novel direction for combination strategies involving epigenetic therapy to provide durable response.

Indexed as

Prostatic Neoplasms, Castration-ResistantReceptors, AndrogenAdaptation, PhysiologicalAndrogen AntagonistsHumansMaleSignal TransductionAndrogen AntagonistsReceptors, Androgen

Identifiers

PMID35993978
PMCPMC10353263
OpenAlexW4226395623

What OpenQuestion holds

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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.