Evidence map›Paper›PMID 41714535›Full record

ArticleDigestive diseases and sciences2026

Persistent Gene Activation as a Molecular Signature of Ulcerative Colitis Progression to Colorectal Cancer.

Yuxiao Ji, Pengchong Li, Yuqi Liu, Dan Shen, Yuanzhen Hao, Yisi Liu, Huixin Song, Wei Sun, Shengtao Zhu, Peng Li and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Digestive diseases and sciences, 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. Article
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

11 authors.

Yuxiao Ji *Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Pengchong Li *Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Yuqi Liu *Department of Rheumatology, Beijing Hospital, National Centre of Gerontology, Institute of Geriatric Medicine, Clinical Immunology Centre, Peking Union Medical College, Chinese Academy of Medical Sciences, No. 1 Dahua Road, Dongdan, Dongcheng District, Beijing, China.
Dan ShenDepartment of Rheumatology, Beijing Hospital, National Centre of Gerontology, Institute of Geriatric Medicine, Clinical Immunology Centre, Peking Union Medical College, Chinese Academy of Medical Sciences, No. 1 Dahua Road, Dongdan, Dongcheng District, Beijing, China.
Yuanzhen HaoDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Yisi LiuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Huixin SongDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Wei SunDepartment of Rheumatology, Beijing Hospital, National Centre of Gerontology, Institute of Geriatric Medicine, Clinical Immunology Centre, Peking Union Medical College, Chinese Academy of Medical Sciences, No. 1 Dahua Road, Dongdan, Dongcheng District, Beijing, China.
Shengtao ZhuDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China. zhushengtao@ccmu.edu.cn.
Peng LiDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China. lipeng@ccmu.edu.cn.
Shutian ZhangDepartment of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China. zhangshutian@ccmu.edu.cn.

Funding

Beijing Municipal Administration of Hospitals Incubating Program PX20240105Beijing Natural Science Foundation 7244317Capital Medical University Excellent Young Scientists Program B2415Capital Medical University Training Fund CCMU2023ZKYXZ002National Key Research and Development Program of China 2022YFC3602100National Natural Science Foundation of China 81970496National Natural Science Foundation of China 82400606Seed Plan of Beijing Friendship Hospital YYZZ202208
6 · The paper itself

Abstract

introductionUlcerative colitis (UC) is an inflammatory disease characterized by colonic epithelial damage. With prolonged disease duration, the risk of malignant transformation increases significantly. However, the mechanisms driving the progression from chronic inflammation to tumorigenesis remain incompletely understood. This study aimed to identify a set of genes that may contribute to the transition from healthy controls (HC) to UC and ultimately to colitis-associated colorectal cancer (CAC).

methodsWe conducted bioinformatic analysis of four Gene Expression Omnibus (GEO) datasets to identify genes involved in the transitions from HC to UC and from UC to CAC. Functional enrichment and immune infiltration analyses were performed. Immunohistochemistry (IHC) validated the expression of key genes in UC patients. In vitro experiments assessed the effect of IFN-γ and TNF-α stimulation on PDL1 expression in neutrophils.

resultsSeven key genes-S100A8, IL33, MGP, MMP3, CFI, CLU, and CLEC4E-were upregulated during HC to UC and UC to CAC transitions. These genes were linked to neutrophils and pathways like Interferon (IFN)-γ, Tumor Necrosis Factor (TNF)-α and oxidative phosphorylation. Immunohistochemistry in mice confirmed expression levels, with five genes showing statistical significance. Additionally, IFN-γ and TNF-α stimulation significantly increased Programmed Death-Ligand 1 (PD-L1) expression in neutrophils.

conclusionWe identified seven genes that are persistently upregulated during the progression from HC to UC and CAC. These genes influence neutrophils and inflammatory/tumorigenic pathways. The upregulation of PD-L1 in neutrophils suggests that neutrophil-mediated immune suppression may contribute to CAC progression, supporting their potential as molecular markers and therapeutic targets for early intervention in UC-related cancer.

Indexed as

Colitis-Associated NeoplasmsColitis, UlcerativeColorectal NeoplasmsAnimalsDisease ProgressionGene Expression ProfilingGene Expression Regulation, NeoplasticHumansInterferon-gammaMiceNeutrophilsTumor Necrosis Factor-alphaInterferon-gammaTumor Necrosis Factor-alphaBioinformatics analysisColitis-associated colorectal cancerGenesNeutrophilsUlcerative colitis

Identifiers

PMID41714535

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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.