Evidence map›Paper›PMID 40489743›Full record

ArticleHepatology (Baltimore, Md.)2026

Arid1a deficiency promotes hepatocyte hyperpolyploidy and drives intrahepatic cholangiocarcinoma in mice.

Qi Bian, Shu Wang, Zimin Song, Fang Liu, Muqing Cao, Nan Yang, Jun Ying, Jia-Syuan Hu, Xinyuan Xiong, Huiqin Zhu and 5 more

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In one paragraph

Article in Hepatology (Baltimore, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Article
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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

15 authors.

Qi BianDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shu WangDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0009-0000-8104-4088
Zimin SongDepartment of Hepatic Surgery, Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.ORCID 0000-0002-0302-3502
Fang LiuDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Muqing CaoDepartment of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of the Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0002-0352-6548
Nan YangDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jun YingSchool of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jia-Syuan HuDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xinyuan XiongDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Huiqin ZhuDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jun WuDepartment of Laboratory Medicine, Jiading Branch of Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-2515-6418
Jie YangDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-5149-538
Xiaonan WangSchool of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-3759-778
Shunli ShenDepartment of Hepatic Surgery, Center of Hepato-Pancreato-Biliary Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Xuxu SunDepartment of Biochemistry and Molecular Cell Biology, State Key Laboratory of Systems Medicine for Cancer, Shanghai Key Laboratory for Tumor Microenvironment and Inflammation, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-6936-7570

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsIntrahepatic cholangiocarcinomas (ICCs) are aggressive liver tumors with high heterogeneity and limited therapeutic options. Although traditionally thought to arise from biliary cells, recent findings suggest that hepatocytes may also serve as a cellular origin for ICC. However, the mechanisms underlying hepatocyte malignant transformation and ICC initiation remain poorly understood. APPROACH AND

resultsWe employed oncogene-driven and chemically induced ICC murine models, along with cellular models, to recapitulate the transformation of hepatocytes into ICC. Our findings demonstrate that mature hepatocytes undergo a significant hyperpolyploid state during ICC initiation. Hyperpolyploidy promotes aberrant cell division and chromosomal instability, accelerating hepatocyte transformation and ICC onset. Furthermore, we identified the chromatin remodeling factor Arid1a as a critical suppressor of hyperpolyploidy. Arid1a deficiency disrupts mitotic machinery at the centrosome, driving hyperpolyploidization and ICC tumorigenesis.

conclusionsHepatocytes can transform into ICC through a process involving hyperpolyploidization. This study offers new insights into the pathogenesis of ICC, particularly in patients harboring frequent ARID1A mutations.

Indexed as

Bile Duct NeoplasmsCell Transformation, NeoplasticCholangiocarcinomaDNA-Binding ProteinsHepatocytesPolyploidyTranscription FactorsAnimalsDisease Models, AnimalHumansMiceMice, KnockoutArid1a protein, mouseDNA-Binding ProteinsTranscription Factorsintrahepatic cholangiocarcinomapolyploidySWI/SNF

Identifiers

PMID40489743
PMCPMC13178779

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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 OpenQuestion graph.