Evidence map›Paper›PMID 40957478›Full record

ArticleJournal of advanced research2026

Integrative proteomic characterization of human lung adenocarcinoma with KRAS G12 mutations reveals molecular pathogenesis.

Xinyu Shi, Liling Hu, Yongshi Huang, Mei-Fang Zhang, Xingfeng Ying, Xiaoyi Yuan, Nengqiao Wen, Jiangli Lu, Hanchen Zou, Xiaohui Tan and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2026. 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.

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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

14 authors.

Xinyu ShiMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Liling HuMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Yongshi HuangDepartment of Molecular Diagnostics, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Mei-Fang ZhangDepartment of Pathology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Xingfeng YingMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Xiaoyi YuanMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Nengqiao WenDepartment of Pathology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Jiangli LuDepartment of Pathology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
Hanchen ZouMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Xiaohui TanMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Qing-Yu HeMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China.
Fang WangDepartment of Molecular Diagnostics, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou 510060, China. Electronic address: wangfang@sysucc.org.cn.
Hong YangDepartment of Thoracic Surgery, State Key Laboratory of Oncology in South China, Guangdong Esophageal Cancer Institute, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou, China. Electronic address: yanghong@sysucc.org.cn.
Chris Zhiyi ZhangMOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, College of Life Science and Technology, Jinan University, Guangzhou 510632, China. Electronic address: zhangzy@jnu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIntegrated proteogenomic studies of lung adenocarcinoma (LUAD) have provided unique insights with potential clinical effects. Comprehensive proteomic analyses are needed to better understand the molecular landscape of LUAD with KRAS G12 mutations.

objectivesThis study aims to characterize the proteogenomic profile of LUAD with KRAS G12 mutation variants.

methodsWe performed next-generation sequencing (NGS) on 9,479 solid tumors, including 3,523 lung cancers. Proteomic profiling was conducted on 96 LUAD patients with KRAS G12 mutations or wild-type status using liquid chromatography-tandem mass spectrometry (LC-MS/MS). The LUAD tumor immune microenvironment (TIME) was characterized by multiplex immunohistochemistry (mIHC), and protein-protein interactions (PPIs) in KRAS G12-mutant lung cancer cells were mapped using biotin-based proximity labeling.

resultsGenomic analysis revealed heterogeneous KRAS-informed mutational profiles across pan-cancer and lung cancer, with allele-specific resolution for KRAS G12 mutations. Proteomic profiling of KRAS G12-mutant LUAD delineated distinct molecular features and tumor progression hallmarks. Unsupervised clustering identified three molecular subtypes, with the immune modulation subtype (S2) characterized by KRAS G12C enrichment, aggressive clinical features, and the greatest potential benefit from immunotherapy. The immune landscape of LUAD showed increased immune cell infiltration in KRAS G12C-mutant tumors. Additionally, proximal proteomics mapped a landscape of gain-of-interactions driven by KRAS G12 mutations, with ion transporter SLC4A7 emerged as a potential effector in immune modulation in the G12C variant.

conclusionsThis comprehensive proteogenomic study provides insights into the molecular features of LUAD harboring KRAS G12 mutations, which may inform patient stratification and potential therapeutic approaches, pending further clinical validation.

Indexed as

Adenocarcinoma of LungLung NeoplasmsMutationProteomicsProto-Oncogene Proteins p21(ras)FemaleHigh-Throughput Nucleotide SequencingHumansMaleTandem Mass SpectrometryTumor MicroenvironmentKRAS protein, humanProto-Oncogene Proteins p21(ras)KRAS G12 mutationsLung adenocarcinomaProteomics study

Identifiers

PMID40957478
PMCPMC13227296

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.