Evidence map›Paper›PMID 39251326›Full record

ArticleGut2025

Microbiota-induced S100A11-RAGE axis underlies immune evasion in right-sided colon adenomas and is a therapeutic target to boost anti-PD1 efficacy.

Qiming Zhou, Linhan Lei, Junhong Cheng, Junyou Chen, Yuyang Du, Xuehua Zhang, Qing Li, Chuangen Li, Haijun Deng, Chi Chun Wong and 3 more

Abstract read
In one paragraph

Article in Gut, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  14. Potential mechanism ofWorld journal of gastrointestinal oncology · 2025
    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

13 authors.

Qiming ZhouDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0000-0001-9945-0084
Linhan LeiDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0009-0000-1923-5115
Junhong ChengDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0009-0009-2780-247X
Junyou ChenDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0000-0002-8989-0518
Yuyang DuDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0009-0005-2849-8474
Xuehua ZhangDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0000-0002-6923-2008
Qing LiDermatology Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID 0000-0002-0169-8098
Chuangen LiInstitute of Chinese Medical Sciences, University of Macao, Taipa, Macao.ORCID 0000-0002-1977-4298
Haijun DengDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Chi Chun WongInstitute of Digestive Disease, Department of Medicine and Therapeutics, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Sciences, CUHK-Shenzhen Research Institute, The Chinese University of Hong Kong, Hong Kong, Hong Kong SAR, China baixiaowudoctor@foxmail.com gzliguoxin@163.com 18820095121@163.com chichun.wong@cuhk.edu.hk.
Baoxiong ZhuangDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China baixiaowudoctor@foxmail.com gzliguoxin@163.com 18820095121@163.com chichun.wong@cuhk.edu.hk.
Guoxin LiDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China baixiaowudoctor@foxmail.com gzliguoxin@163.com 18820095121@163.com chichun.wong@cuhk.edu.hk.ORCID 0000-0003-2773-7048
Xiaowu BaiDepartment of General Surgery, Guangdong Provincial Key Laboratory of Precision Medicine for Gastrointestinal Tumor, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China baixiaowudoctor@foxmail.com gzliguoxin@163.com 18820095121@163.com chichun.wong@cuhk.edu.hk.ORCID 0000-0001-8377-0518

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumourigenesis in right-sided and left-sided colons demonstrated distinct features.

objectiveWe aimed to characterise the differences between the left-sided and right-sided adenomas (ADs) representing the early stage of colonic tumourigenesis.

designSingle-cell and spatial transcriptomic datasets were analysed to reveal alterations between right-sided and left-sided colon ADs. Cells, animal experiments and clinical specimens were used to verify the results.

resultsSingle-cell analysis revealed that in right-sided ADs, there was a significant reduction of goblet cells, and these goblet cells were dysfunctional with attenuated mucin biosynthesis and defective antigen presentation. An impairment of the mucus barrier led to biofilm formation in crypts and subsequent bacteria invasion into right-sided ADs. The regions spatially surrounding the crypts with biofilm occupation underwent an inflammatory response by lipopolysaccharide (LPS) and an apoptosis process, as revealed by spatial transcriptomics. A distinct S100A11

conclusionOur findings unravelled that dysfunctional goblet cells and consequential bacterial translocation activated the S100A11-RAGE axis in right-sided colon ADs, which recruits MDSCs to promote immune evasion. Targeting this axis by Azeliragon improves the efficacy of immunotherapy in colon cancer.

Indexed as

AdenomaColonic NeoplasmsGastrointestinal MicrobiomeImmune EvasionReceptor for Advanced Glycation End ProductsS100 ProteinsAnimalsGoblet CellsHumansImmune Checkpoint InhibitorsMiceMyeloid-Derived Suppressor CellsProgrammed Cell Death 1 ReceptorImmune Checkpoint InhibitorsProgrammed Cell Death 1 ReceptorReceptor for Advanced Glycation End ProductsS100 Proteinsbacterial translocationcancercolonic adenomascolonic microfloraimmunotherapy

Identifiers

PMID39251326
PMCPMC11874379

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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 OpenQuestion graph.