ArticleCancer science2003
A novel inflammation-related mouse colon carcinogenesis model induced by azoxymethane and dextran sodium sulfate.
Article in Cancer science, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 372 papers.
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Who cites it
372 citing papers in PubMed, 722 citations in OpenAlex.
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- The intervention of NLRP3 inflammasome inhibitor: oridonin against azoxymethane and dextran sulfate sodium-induced colitis-associated colorectal cancer in male BALB/c mice.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- LncRNA HOTTIP modulated by Hedgehog signaling drives colorectal cancer progression by promoting HUWE1-mediated ubiquitin‒proteasome degradation of p53.Cell death & disease · 2025Article
- Gut commensal bacteria influence colorectal cancer development by modulating immune response in AOM/DSS-treated mice.Microbiology spectrum · 2025Article
- The IL-22-oncostatin M axis promotes intestinal inflammation and tumorigenesis.Nature immunology · 2025Article
- Hypoxia-induced Wnt5a-secreting fibroblasts promote colon cancer progression.Nature communications · 2025Article
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- Review
312 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To develop an efficient animal model for colitis-related carcinogenesis, male Crj: CD-1 (ICR) mice were given a single intraperitoneal administration (10 mg/kg body weight) of a genotoxic colonic carcinogen, azoxymethane (AOM), and a 1-week oral exposure (2% in drinking water) to a non-genotoxic carcinogen, dextran sodium sulfate (DSS), under various protocols. At week 20, colonic neoplasms (adenocarcinomas, 100% incidence with 5.60 +/- 2.42 multiplicity; and adenomas, 38% incidence with 0.20 +/- 0.40 multiplicity) with dysplastic lesions developed in mice treated with AOM followed by DSS. Protocols in which AOM was given during or after DSS administration induced a few tubular adenomas or no tumors in the colon. Immunohistochemical investigation of such dysplasias and neoplasms revealed that all lesions were positive for beta-catenin, cyclooxygenase-2 and inducible nitric oxide synthase, but did not show p53 immunoreactivity. The results indicate that 1-week administration of 2% DSS after initiation with a low dose of AOM exerts a powerful tumor-promoting activity in colon carcinogenesis in male ICR mice, and may provide a novel mouse model for investigating colitis-related colon carcinogenesis and for identifying xenobiotics with modifying effects.
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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.