Evidence map›Paper›PMID 40946102›Full record

ReviewOncogene2025

NRF2 immunobiology in cancer: implications for immunotherapy and therapeutic targeting.

Harit Panda, Natalie G Rowland, Caroline M Krall, Brittany M Bowman, Michael B Major, Paul Zolkind

Abstract readReview
In one paragraph

Review in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
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  4. Article
  5. Review
  6. Article
  7. Article
  8. T cell-intrinsic integrated stress response: friend, foe, or frill?Journal of the National Cancer Center · 2026
    Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Review
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  15. 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

6 authors.

Harit PandaDepartment of Otolaryngology, Washington University School of Medicine, St. Louis, MO, USA.
Natalie G RowlandDepartment of Otolaryngology, Washington University School of Medicine, St. Louis, MO, USA.
Caroline M KrallDepartment of Otolaryngology, Washington University School of Medicine, St. Louis, MO, USA.
Brittany M BowmanDepartment of Biological Chemistry, Center for RNA Biomedicine, Rogel Cancer Center, University of Michigan Medical School, Ann Arbor, MI, USA.
Michael B MajorDepartment of Otolaryngology, Washington University School of Medicine, St. Louis, MO, USA. bmajor@wustl.edu.ORCID 0000-0002-6753-8513
Paul ZolkindDepartment of Otolaryngology, Washington University School of Medicine, St. Louis, MO, USA. pzolkind@wustl.edu.ORCID 0000-0002-9475-1686

Funding

Drugging NRF2 to improve radiation therapy in head and neck squamous cell carcinomaR01CA290809 · NCI · WASHINGTON UNIVERSITY · PI Michael Benjamin Major, Bernard E. Weissman · 2025 to 2026
$1.3M
BLRD VA IK2 BX006120NCI NIH HHS R01 CA290809U.S. Department of Veterans Affairs (Department of Veterans Affairs) BX006120
6 · The paper itself

Abstract

Nuclear factor erythroid 2-related factor 2 (NRF2) is a transcription factor that acts as a key regulator in cellular defense mechanisms against oxidative stress and xenobiotics. NRF2 modulates the expression of over 200 genes involved in antioxidant response, drug metabolism, and cellular resilience. Constitutive activation of NRF2 is a common event in cancer and recent advances provide remarkable insights into the role of NRF2 in oncogenesis, immune evasion, and treatment resistance. This review aims to provide a comprehensive overview of the role of NRF2 in shaping the tumor immune microenvironment and the impact this has on clinical outcomes and treatment opportunities. Across multiple tumor subtypes, the activation of NRF2 is associated with impaired responses to anti-PD1 immunotherapy. Mechanistic insights from genetically engineered mouse models, in vitro studies, and clinical trial samples demonstrate how NRF2 activity supports cell resiliency, diminishes cytotoxic immune responses, and promotes metabolic reprogramming. This also provides a vulnerability which can be targeted through novel drug therapy and future directions will include development of optimal combination strategies to target tumor dependencies while minimizing toxicity and systemic off-target immune related effects.

Indexed as

ImmunotherapyNeoplasmsNF-E2-Related Factor 2AnimalsHumansMolecular Targeted TherapyTumor MicroenvironmentNFE2L2 protein, humanNF-E2-Related Factor 2

Identifiers

PMID40946102
PMCPMC12454149

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.