Evidence map›Paper›PMID 41541668›Full record

ReviewiScience2026

Tumor suppressor genes and KRAS G12C inhibitor resistance in non-small cell lung cancer.

Linsha Zhu, Xiangbo Jia, Lei Xu, Li Chen, Xiangning Fu, Hua Yan, Bo Ai, Shu Peng

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. CRISPR Interference to Inhibit Oncogenes for Cancer Therapy.International journal of molecular sciences · 2026
    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

8 authors.

Linsha ZhuDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Xiangbo JiaDepartment of Thoracic Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, School of clinical medicine, Henan University, Zhengzhou, Henan, P.R. China.
Lei XuDepartment of Thoracic Surgery, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, School of clinical medicine, Henan University, Zhengzhou, Henan, P.R. China.
Li ChenDepartment of Breast Surgical Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, P.R. China.
Xiangning FuDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Hua YanDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Bo AiDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
Shu PengDepartment of Thoracic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

KRAS G12C inhibitors (G12Cis) have revolutionized the treatment of cancers driven by this historically undruggable mutation, offering unprecedented clinical responses in non-small cell lung cancer (NSCLC) and other malignancies. However, both primary and acquired resistance rapidly curtail their efficacy. Emerging clinical and preclinical evidence underscores the heterogeneity of resistance mechanisms. Strikingly, in KRAS-driven NSCLC, a common phenomenon is co-mutations in tumor suppressor genes (TSGs), which orchestrate resistance through multifaceted pathways such as sustained proliferation, metabolic reprogramming, phenotypic plasticity, and immune microenvironment remodeling. Accordingly, this review summarizes relevant reasons underlying diverse resistant mechanisms in KRAS G12C-mutated NSCLC, with an emphasis on deciphering the mechanism of tumor suppressor gene (TSG) alterations serving as key mediators linking oncogenic KRAS dependency to therapeutic resistance. Our research continued to discuss relevant preclinical models to facilitate the advancement of the study of these resistance mechanisms.

Indexed as

CancerGene networkTherapeutics

Identifiers

PMID41541668
PMCPMC12803867

What OpenQuestion holds

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LicenceCC BY
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.