Evidence map›Paper›PMID 34102289›Full record

ReviewSeminars in cancer biology2021

Targeting NRF2 to treat cancer.

Jared Sivinski, Donna D Zhang, Eli Chapman

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in cancer biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
4.9field-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

45 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  3. Immunological drivers of oxidative stress in glaucoma: implications for antioxidant therapy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
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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

3 authors at 1 institution in 1 country.

Jared SivinskiDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, 85721, USA.
Donna D ZhangDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, 85721, USA.
Eli ChapmanDepartment of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, AZ, 85721, USA. Electronic address: chapman@pharmacy.arizona.edu.
University of Arizona · US

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
NRF Transcription Factors in Environmental Stress and Disease InterventionR35ES031575 · NIEHS · UNIVERSITY OF FLORIDA · PI Donna D Zhang · 2020 to 2026
$7.1M
CHEMISTRY-BIOLOGY INTERFACE TRAINING PROGRAMT32GM008804 · NIGMS · UNIVERSITY OF ARIZONA · PI MONTFORT, WILLIAM R. · 2003 to 2023
$3.9M
Selective modulation of bacterial chaperonins by targeting novel small molecule binding sitesR01GM120350 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI JOHNSON, STEVEN MICHAEL · 2017 to 2021
$2.3M
Stress response, p97, and Nrf2 in arsenic-mediated toxicityR01ES023758 · NIEHS · UNIVERSITY OF ARIZONA · PI CHAPMAN, ELI, ZHANG, DONNA D · 2014 to 2018
$1.6M
Redox and Protein Homeostasis in Arsenic TumorigenicityR01ES031463 · NIEHS · UNIVERSITY OF FLORIDA · PI CHAPMAN, ELI · 2020 to 2024
$1.6M
NIEHS NIH HHS P30 ES006694NIEHS NIH HHS R01 ES023758NIEHS NIH HHS R01 ES031463NIEHS NIH HHS R35 ES031575NIGMS NIH HHS R01 GM120350NIGMS NIH HHS T32 GM008804
6 · The paper itself

Abstract

NRF2 is a basic leucine zipper (bZip) transcription factor that is the master regulator of redox homeostasis. Under basal conditions, the cellular level of NRF2 is low due to a posttranslational regulation by the ubiquitin proteasome system (UPS). But, when an organism is challenged with oxidative or xenobiotic stress, the NRF2 pathway is activated by inhibition of the E3 ubiquitin ligase complex that normally marks NRF2 for destruction. For several decades, researchers have searched for molecules that can intentionally activate NRF2, as this was shown to be a means to prevent certain diseases, at least in animal models. In the present era, there are many compounds known to activate the NRF2 pathway including natural products and synthetic compounds, covalent and non-covalent compounds, and others. However, it was also revealed that like many protective pathways, the NRF2 pathway has a dark side. Just as NRF2 can protect normal cells from damage, it can protect malignant cells from damage. As cells transform, they are exposed to many stressors and aberrant upregulation of NRF2 can facilitate transformation and it can help cancer cells to grow, to spread, and to resist treatment. For this reason, researchers are also interested in the discovery and development of NRF2 inhibitors. In the present review, we will begin with a general discussion of NRF2 structure and function, we will discuss the latest in NRF2 non-covalent activators, and we will discuss the current state of NRF2 inhibitors.

Indexed as

NeoplasmsAnimalsHumansMolecular Targeted TherapyNF-E2-Related Factor 2NF-E2-Related Factor 2CancerChemopreventionNRF2Transcription factor

Identifiers

PMID34102289
PMCPMC8627924
OpenAlexW3169306949

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.