Evidence map›Paper›PMID 19793802›Full record

ReviewCarcinogenesis2010

Nrf2: friend or foe for chemoprevention?

Thomas W Kensler, Nobunao Wakabayashi

Open access · bronzeAbstract readReview
In one paragraph

Review in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 238 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
238citing papers in PubMed, 1 pooled it
14.9field-weighted citation impact, top 1% 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

238 citing papers in PubMed, 1 synthesis or guideline pooled it, 488 citations in OpenAlex.

  1. Pooled it
  2. Prevention of Carcinogen-Induced Oral Cancer by Sulforaphane.Cancer prevention research (Philadelphia, Pa.) · 2016
    Trial
  3. Trial
  4. Review
  5. Hepatocyte-SpecificAntioxidants (Basel, Switzerland) · 2026
    Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. The Anti-AGEing and RAGEing Potential of Isothiocyanates.Molecules (Basel, Switzerland) · 2024
    Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. FOXO transcription factors as mediators of stress adaptation.Nature reviews. Molecular cell biology · 2024
    Review
  19. Review
  20. Article

178 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Thomas W KenslerDepartment of Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, 615 North Wolfe Street, Baltimore, MD 21205, USA. tkensler@jhsph.edu
Nobunao Wakabayashi
University of Pittsburgh · US

Funding

VACCINES--A NEW PARADIGM FOR BREAST CANCERP50CA088843 · NCI · JOHNS HOPKINS UNIVERSITY · PI DAVIDSON, NANCY ELLEN · 2000 to 2010
$27.8M
Validation and Application of Risk, Biomarkers in Human StudiesP01ES006052 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI GROOPMAN, JOHN D · 1993 to 2012
$22.6M
Molecular Mechanisms of Chemoprevention: NRF2 SignalingR01CA039416 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KENSLER, THOMAS W · 1985 to 2013
$7.0M
Role of Nrf2 Cross-Talk in Cancer ChemopreventionR01CA094076 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KENSLER, THOMAS W · 2002 to 2015
$5.5M
NCI NIH HHS P50 CA088843NCI NIH HHS R01 CA039416NCI NIH HHS R01 CA094076NIEHS NIH HHS P01 ES06052
6 · The paper itself

Abstract

Health reflects the ability of an organism to adapt to stress. Stresses--metabolic, proteotoxic, mitotic, oxidative and DNA-damage stresses--not only contribute to the etiology of cancer and other chronic degenerative diseases but are also hallmarks of the cancer phenotype. Activation of the Kelch-like ECH-associated protein 1 (KEAP1)-NF-E2-related factor 2 (NRF2)-signaling pathway is an adaptive response to environmental and endogenous stresses and serves to render animals resistant to chemical carcinogenesis and other forms of toxicity, whilst disruption of the pathway exacerbates these outcomes. This pathway can be induced by thiol-reactive small molecules that demonstrate protective efficacy in preclinical chemoprevention models and in clinical trials. However, mutations and epigenetic modifications affecting the regulation and fate of NRF2 can lead to constitutive dominant hyperactivation of signaling that preserves rather than attenuates cancer phenotypes by providing selective resistance to stresses. This review provides a synopsis of KEAP1-NRF2 signaling, compares the impact of genetic versus pharmacologic activation and considers both the attributes and concerns of targeting the pathway in chemoprevention.

Indexed as

ChemopreventionHumansIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1NF-E2-Related Factor 2Signal TransductionIntracellular Signaling Peptides and ProteinsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1NFE2L2 protein, humanNF-E2-Related Factor 2

Identifiers

PMID19793802
PMCPMC2802668
OpenAlexW2122116064

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.