Evidence map›Paper›PMID 41786878›Full record

ArticleOncogene2026

KRAS-extrachromosomal DNA drives intratumoral heterogeneity in gastric cancer.

Rong Guan, Chenxi Li, Xinchun Dai, Yanyan Wang, Yiyuan Zhang, Xiao Liang, Shan Yu, Zhizhou Li, Kexian Dong, Mengdi Cai and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 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. 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

16 authors.

Rong Guan *Department of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Chenxi Li *Department of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Xinchun Dai *Department of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Yanyan WangDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Yiyuan ZhangDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Xiao LiangDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Shan YuDepartment of Pathology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Zhizhou LiDepartment of General Surgery, the Fifth Affiliated Hospital of Harbin Medical University, Daqing, China.
Kexian DongDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Mengdi CaiDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Jie WuDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China.
Xueyuan JiaDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China. jiaxueyuan@hrbmu.edu.cn.
Hao WangDepartment of Hepatopancreatobiliary Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, China. wanghao@hrbmu.edu.cn.
Dapeng HaoDepartment of Pathology, School of Basic Medical Sciences, Harbin Medical University, Harbin, China. dapenghao@hrbmu.edu.cn.
Songbin FuDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China. fusb@ems.hrbmu.edu.cn.
Wenjing SunDepartment of Medical Genetics, School of Basic Medical Sciences, Harbin Medical University, Harbin, China. sunwj@ems.hrbmu.edu.cn.ORCID http://orcid.org/0000-0001-5638-5892

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extrachromosomal DNA (ecDNA), autonomously replicating circular DNA outside the chromosomes, exists as critical oncogene driver in approximately 20% of all tumors. Massive ecDNA amplification and its asymmetric segregation during mitotic drive high level oncogene amplification and contribute to tumor heterogeneity. Gastric cancer exhibits a high frequency of ecDNA occurrence. KRAS, a key oncogene in multiple cancers, is frequently amplified in gastric cancer; however, its functional implications via ecDNA remain largely understudied. In this study, we performed whole-genome sequencing and single-cell RNA sequencing on a gastric cancer sample to identify genomic amplification and transcription driven by ecDNA. We identified KRAS-ecDNA in gastric cancer, which exhibited significantly elevated KRAS expression and pronounced transcriptional heterogeneity. Functionally, ecDNA_High cells showed enhanced ribosome biogenesis, upregulated DNA repair pathways, differential activation of transcription factors,and reduced MHC-II signaling, indicating potential immune evasion. Drug response predictions suggested that KRAS-ecDNA_High cells are sensitive to MAPK inhibitors and upstream receptor inhibitors, despite showing broad resistance to conventional chemotherapies. Our study uncovers the critical role of KRAS-ecDNA in gastric cancer. These findings provide a rationale for targeting ecDNA-driven oncogenic programs and offer targeted strategies to combat ecDNA-mediated oncogenic evolution.

Indexed as

Extrachromosomal DNAProto-Oncogene Proteins p21(ras)Stomach NeoplasmsCell Line, TumorGene AmplificationGene Expression Regulation, NeoplasticHumansExtrachromosomal DNAKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID41786878

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