Evidence map›Paper›PMID 41871943›Full record

ArticleGut2026

Dysbiotic microbiota trigger colitis-associated colorectal cancer and imprint a distinctive bile acid profile in a PSC-IBD model.

Muyiwa Awoniyi, Mohamed El Hag, Josue Hernandez, Qijun Yang, Nicholas Evans, Ina Nemet, Billy Ngo, Deniz Coskuner, Julie Zhou, Morgan Farmer and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Gut, 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

15 authors.

Muyiwa AwoniyiCenter for Gastrointestinal Biology and Disease, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA muyiwa7@gmail.com.ORCID http://orcid.org/0000-0002-5811-070X
Mohamed El HagDiagnostics Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Josue HernandezDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA.
Qijun YangDigestive Disease Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Nicholas EvansDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA.ORCID http://orcid.org/0000-0002-9576-4454
Ina NemetDepartment of Heart, Blood and Kidney Research, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA.
Billy NgoCenter for Gastrointestinal Biology and Disease, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Deniz CoskunerCenter for Gastrointestinal Biology and Disease, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Julie ZhouDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA.ORCID http://orcid.org/0000-0002-1533-5183
Morgan FarmerCenter for Gastrointestinal Biology and Disease, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Lianyong SuDivision of Gastroenterology and Hepatology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA.
Huiping ZhouDivision of Gastroenterology and Hepatology, Virginia Commonwealth University School of Medicine, Richmond, Virginia, USA.ORCID http://orcid.org/0000-0002-0050-372X
Jeffery RoachUNC Microbiome Core, Center for Gastrointestinal Biology and Disease, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.
Thaddeus StappenbeckDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, Ohio, USA.ORCID http://orcid.org/0000-0002-6023-3901
R Balfour SartorCenter for Gastrointestinal Biology and Disease, The University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA.ORCID http://orcid.org/0000-0002-7820-632X

Funding

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Venkata Saroja Voruganti · 1999 to 2026
$31.6M
PILOT AND FEASIBILITY STUDIESP30DK034987 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ROBERT S. SANDLER · 1985 to 2026
$30.5M
Role of IL-10 in APC Regulation of Protective vs. Pathogenic T Cell Responses toP01DK094779 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHEIKH, SHEHZAD Z. · 2013 to 2023
$17.9M
National Gnotobiotic Rodent Resource CenterP40OD010995 · OD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Ryan B Sartor · 2012 to 2026
$9.7M
GASTROENTEROLOGY RESEARCH TRAININGT32DK007737 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHEHZAD Z. SHEIKH · 1996 to 2026
$7.8M
Extending experimental evolutionary game theory in cancer in vivo to enable clinical translation: integrating spatio-temporal dynamics using mathematical modelingU01CA280829 · NCI · CLEVELAND CLINIC LERNER COM-CWRU · PI Andriy Marusyk, Jacob Gardinier Scott · 2023 to 2026
$2.6M
Circular RNAs in Cholestatic Liver DiseasesR01DK139587 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI HUIPING ZHOU · 2024 to 2026
$2.2M
BLRD VA I01 BX005730BLRD VA IK6 BX004477BLRD VA IS1 BX004777NCI NIH HHS U01 CA280829NIDDK NIH HHS P01 DK094779NIDDK NIH HHS P30 DK034987NIDDK NIH HHS P30 DK056350NIDDK NIH HHS R01 DK139587NIDDK NIH HHS T32 DK007737NIH HHS P40 OD010995
6 · The paper itself

Abstract

backgroundPrimary sclerosing cholangitis-associated UC (PSC-UC) carries excess colorectal neoplasia despite often mild-appearing endoscopy, implicating persistent microscopic inflammation and microbiota-bile acid (BA) dysfunction.

objectiveTo test whether PSC-UC neoplasia is driven by transferable microbiota-mediated inflammation linked to secondary BA loss.

designSurveillance colonoscopies (2012-2022) from PSC-UC (n=251) and UC-only (n=8839) were compared for segmental endoscopic/histological activity and dysplasia. We generated multidrug resistance protein 2 (MDR2)

resultsPSC-UC showed greater inflammatory activity and a right-shifted dysplasia burden versus UC-only. Under specific-pathogen-free conditions, DKO mice developed early right-predominant colitis and multifocal dysplasia progressing with age. DKO communities were depleted of 7α-dehydroxylation capacity with near absence of deoxycholic and lithocholic acids and no enrichment of canonical bacterial genotoxins. GF DKO mice were protected, whereas live DKO donor FMT reinstated severe colitis and dysplasia; sterile-filtered stool supernatant was inactive. IL-10

conclusionPSC-UC neoplasia associates with transmissible microbiota-dependent inflammation and secondary BA deficiency. Controlled restoration of BA-transforming microbial functions, rather than indiscriminate secondary BA replacement, is a rational translational direction.

Indexed as

Bile Acids and SaltsCholangitis, SclerosingColitis-Associated NeoplasmsColitis, UlcerativeColorectal NeoplasmsDysbiosisGastrointestinal MicrobiomeAnimalsColitisDisease Models, AnimalFecal Microbiota TransplantationHumansMaleMiceMice, Inbred C57BLMice, KnockoutBile Acids and SaltsBILE ACIDCOLON CARCINOGENESISGASTROINTESTINAL MICROBIOMEINFLAMMATORY BOWEL DISEASEPRIMARY SCLEROSING CHOLANGITIS

Identifiers

PMID41871943
PMCPMC13479688

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.