Evidence map›Paper›PMID 40890297›Full record

ArticleBritish journal of cancer2025

Systemic activation of NRF2 contributes to the therapeutic efficacy of clinically-approved KRAS-G12C anti-cancer drugs.

Liam Baird, Lin Zhang, Takanori Hidaka, Lyu Xi, Ke Wang, Keiko Tateno, Tatsuro Iso, Takafumi Suzuki, Kazuki Kumada, Fumiki Katsuoka and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. 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

12 authors.

Liam BairdDepartment of Biochemistry and Molecular Biology, Tohoku University, Tohoku Medical Megabank Organization, Sendai, Japan. liambaird@med.tohoku.ac.jp.
Lin ZhangTohoku Medical Megabank Organization, Tohoku University, Sendai, Miyagi, Japan.
Takanori HidakaTohoku Medical Megabank Organization, Tohoku University, Sendai, Miyagi, Japan.
Lyu XiDepartment of Biochemistry and Molecular Biology, Tohoku University, Tohoku Medical Megabank Organization, Sendai, Japan.
Ke WangDepartment of Biochemistry and Molecular Biology, Tohoku University, Tohoku Medical Megabank Organization, Sendai, Japan.
Keiko TatenoTohoku Medical Megabank Organization, Tohoku University, Sendai, Miyagi, Japan.
Tatsuro IsoDepartment of Biochemistry and Molecular Biology, Tohoku University, Tohoku Medical Megabank Organization, Sendai, Japan.
Takafumi SuzukiDepartment of Biochemistry and Molecular Biology, Tohoku University, Tohoku Medical Megabank Organization, Sendai, Japan.
Kazuki KumadaTohoku Medical Megabank Organization, Tohoku University, Sendai, Miyagi, Japan.ORCID http://orcid.org/0000-0002-2970-7742
Fumiki KatsuokaAdvanced Research Center for Innovations in Next-Generation Medicine (INGEM), Tohoku University, Sendai, Japan.
Kengo KinoshitaTohoku Medical Megabank Organization, Tohoku University, Sendai, Miyagi, Japan.
Masayuki YamamotoDepartment of Biochemistry and Molecular Biology, Tohoku University, Tohoku Medical Megabank Organization, Sendai, Japan. masiyamamoto@med.tohoku.ac.jp.ORCID http://orcid.org/0000-0002-9073-9436

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) 19H05649MEXT | Japan Society for the Promotion of Science (JSPS) 19K16512
6 · The paper itself

Abstract

backgroundThe development and clinical success of KRAS

methodsA broad range of techniques, including genetic knockouts, scRNA-seq and surface plasmon resonance, were used to determine the effect of KRAS

resultsAt physiologically-relevant concentrations, both of the clinically-approved KRAS

conclusionsThe activation of NRF2 by KRAS-G12C inhibitors represents a unique example of anti-cancer drugs which positively regulate the activity of a protein which is normally considered to be an oncogene. In both the malignant cells of the tumour and immune cells within the microenvironment, activation of NRF2 by electrophilic KRAS inhibitors positively contributes to the clinical efficacy of these drugs by promoting anti-cancer immunity. This unprecedented situation, in which the NRF2-dependent oxidative stress response is induced globally within cancer patients, has a number of important clinical implications, particularly in relation to ongoing combination chemotherapy clinical trials, as well as for selecting patient populations which may derive the most benefit from G12Ci anti-cancer drugs.

Indexed as

Antineoplastic AgentsLung NeoplasmsNF-E2-Related Factor 2Proto-Oncogene Proteins p21(ras)AnimalsCell Line, TumorHumansKelch-Like ECH-Associated Protein 1MiceMutationPiperazinesPyridinesPyrimidinesAntineoplastic AgentsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1KRAS protein, humanNFE2L2 protein, humanNF-E2-Related Factor 2PiperazinesProto-Oncogene Proteins p21(ras)PyridinesPyrimidinessotorasib

Identifiers

PMID40890297
PMCPMC12572401

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.