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Article

Bacterial infection promotes colon tumorigenesis in Apc(Min/+) mice.

The Journal of infectious diseases - 15 Jul 2001

Newman J V, Kosaka T, Sheppard B J, Fox J G, Schauer D B

Abstract excerpt

The Min mouse, which has a germ line mutation in 1 allele of the Apc tumor suppressor gene, is a model for the early steps in human colorectal cancer. Helicobacter pylori infection, a known risk factor for gastric cancer in humans, causes chronic inflammation and increased epithelial cell proliferation in the stomach. Infection with the bacterium Citrobacter rodentium is known to increase epithelial cell...

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Identifiers

PMID: 11424022
DOI: 10.1086/321998

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Research trail→

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Bacterial infection promotes colon tumorigenesis in Apc(Min/+) mice.PMID 11424022Read ↗

Helicobacter hepaticus infection promotes colon tumorigenesis in the BALB/c-Rag2(-/-) Apc(Min/+) mouse.Semantic proximity Read ↗

Induction of inflammatory bowel disease accelerates adenoma formation in Min +/- mice.Semantic proximity Read ↗

ApcMin, a mutation in the murine Apc gene, predisposes to mammary carcinomas and focal alveolar hyperplasias.Semantic proximity Read ↗

Altered Interactions between the Gut Microbiome and Colonic Mucosa Precede Polyposis in APCMin/+ Mice.Semantic proximity Read ↗

Multistep carcinogenesis of the colon in Apc(Min/+) mouse.Semantic proximity Read ↗

Intestinal immune responses in wild-type and Apcmin/+ mouse, a model for colon cancer.Semantic proximity Read ↗

Winnie-APCMin/+ Mice: A Spontaneous Model of Colitis-Associated Colorectal Cancer Combining Genetics and Inflammation.Semantic proximity Read ↗

Qualitative and quantitative relationship between dysplastic aberrant crypt foci and tumorigenesis in the Min/+ mouse colon.Semantic proximity Read ↗

Helicobacter infection is required for inflammation and colon cancer in SMAD3-deficient mice.Semantic proximity Read ↗

A resistant genetic background leading to incomplete penetrance of intestinal neoplasia and reduced loss of heterozygosity in ApcMin/+ mice.Semantic proximity Read ↗

Generation of a unique strain of multiple intestinal neoplasia (Apc+/Min‐FCCC) mice with significantly increased numbers of colorectal adenomasSemantic proximity Read ↗

Loss of functional Fas ligand enhances intestinal tumorigenesis in the Min mouse model.Semantic proximity Read ↗

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