F4/80


Journal

Gastroenterology
ISSN: 1528-0012
Titre abrégé: Gastroenterology
Pays: United States
ID NLM: 0374630

Informations de publication

Date de publication:
04 2023
Historique:
received: 15 05 2022
revised: 15 12 2022
accepted: 03 01 2023
pmc-release: 01 04 2024
pubmed: 13 1 2023
medline: 28 3 2023
entrez: 12 1 2023
Statut: ppublish

Résumé

Colorectal cancer is a leading cause of cancer death, and a major risk factor is chronic inflammation. Despite the link between colitis and cancer, the mechanism by which inflammation leads to colorectal cancer is not well understood. To investigate whether different forms of inflammation pose the same risk of cancer, we compared several murine models of colitis (dextran sodium sulfate [DSS], 2,4,6-trinitrobenzene sulfonic acid, 4-ethoxylmethylene-2-phenyloxazol-5-one, Citrobacter rodentium, Fusobacterium nucleatum, and doxorubicin) with respect to their ability to lead to colonic tumorigenesis. We attempted to correlate the severity of colitis and inflammatory profile with the risk of tumorigenesis in both azoxymethane-dependent and Dclk1/APC DSS colitis reproducibly led to colonic tumors in both mouse models of colitis-associated cancer. In contrast, all other forms of colitis did not lead to cancer. When compared with the colitis not associated with tumorigenesis, DSS colitis was characterized by significantly increased CD11b We have identified CD11b

Sections du résumé

BACKGROUND & AIMS
Colorectal cancer is a leading cause of cancer death, and a major risk factor is chronic inflammation. Despite the link between colitis and cancer, the mechanism by which inflammation leads to colorectal cancer is not well understood.
METHODS
To investigate whether different forms of inflammation pose the same risk of cancer, we compared several murine models of colitis (dextran sodium sulfate [DSS], 2,4,6-trinitrobenzene sulfonic acid, 4-ethoxylmethylene-2-phenyloxazol-5-one, Citrobacter rodentium, Fusobacterium nucleatum, and doxorubicin) with respect to their ability to lead to colonic tumorigenesis. We attempted to correlate the severity of colitis and inflammatory profile with the risk of tumorigenesis in both azoxymethane-dependent and Dclk1/APC
RESULTS
DSS colitis reproducibly led to colonic tumors in both mouse models of colitis-associated cancer. In contrast, all other forms of colitis did not lead to cancer. When compared with the colitis not associated with tumorigenesis, DSS colitis was characterized by significantly increased CD11b
CONCLUSIONS
We have identified CD11b

Identifiants

pubmed: 36634827
pii: S0016-5085(23)00011-2
doi: 10.1053/j.gastro.2023.01.002
pmc: PMC10038892
mid: NIHMS1865714
pii:
doi:

Substances chimiques

Azoxymethane MO0N1J0SEN
Dextran Sulfate 9042-14-2
Ly-6C antigen, mouse 0

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

593-609.e13

Subventions

Organisme : NIDDK NIH HHS
ID : U01 DK085532
Pays : United States
Organisme : NIDDK NIH HHS
ID : U01 DK103155
Pays : United States
Organisme : NIDDK NIH HHS
ID : U24 DK085532
Pays : United States

Informations de copyright

Copyright © 2023 AGA Institute. Published by Elsevier Inc. All rights reserved.

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Auteurs

Alice E Shin (AE)

Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Department of Medicine, Western University, London, Ontario, Canada.

Yodit Tesfagiorgis (Y)

Department of Microbiology and Immunology, Western University, London, Ontario, Canada.

Frederikke Larsen (F)

Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Department of Medicine, Western University, London, Ontario, Canada.

Mathieu Derouet (M)

Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Department of Medicine, Western University, London, Ontario, Canada.

Peter Y F Zeng (PYF)

Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Department of Otolaryngology and Head and Neck Surgery, Western University, London, Ontario, Canada.

Hayley J Good (HJ)

Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Department of Medicine, Western University, London, Ontario, Canada.

Liyue Zhang (L)

Department of Medicine, Western University, London, Ontario, Canada.

Mara R Rubinstein (MR)

Section of Oral, Diagnostic and Rehabilitation Sciences, College of Dental Medicine, Columbia University Irving Medical Center, New York, New York.

Yiping W Han (YW)

Section of Oral, Diagnostic and Rehabilitation Sciences, College of Dental Medicine, Columbia University Irving Medical Center, New York, New York; Departments of Microbiology & Immunology and Medicine (Medical Sciences), Columbia University Irving Medical Center, New York, New York.

Steven M Kerfoot (SM)

Department of Microbiology and Immunology, Western University, London, Ontario, Canada.

Anthony C Nichols (AC)

Department of Otolaryngology and Head and Neck Surgery, Western University, London, Ontario, Canada.

Yoku Hayakawa (Y)

Department of Gastroenterology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan.

Christopher J Howlett (CJ)

Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada.

Timothy C Wang (TC)

Department of Medicine, Columbia University Irving Medical Center, New York, New York.

Samuel Asfaha (S)

Department of Pathology and Laboratory Medicine, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada; Department of Medicine, Western University, London, Ontario, Canada. Electronic address: sasfaha2@uwo.ca.

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Classifications MeSH