Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Mlh1 deficiency enhances several phenotypes of Apc(Min)/+ mice.

Oncogene - 25 May 2000

Shoemaker A R, Haigis K M, Baker S M, Dudley S, Liskay R M, Dove W F

Abstract excerpt

Defects in APC and DNA mismatch repair genes are associated with a strong predisposition to colon cancer in humans, and numerous mouse strains with mutations in these genes have been generated. In this report we describe the phenotype of Min/+ Mlh1-/- mice. We find that these doubly mutant mice develop more than three times the number of intestinal adenomas compared to Min/+ Mlh1+/+ or +/- mice but that these...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adaptor Proteins, Signal Transducing
Share to Adenomatous Polyposis Coli Protein

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Base Pair Mismatch

Share to Cytoskeletal Proteins

Share to Intestinal Neoplasms

Share to Mice, Mutant Strains

Share to MutL Protein Homolog 1

Share to Neoplasm Proteins

Source

Identifiers

PMID: 10851078
DOI: 10.1038/sj.onc.1203574

Genes

APC

Provenance

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

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Mlh1 deficiency enhances several phenotypes of Apc(Min)/+ mice.PMID 10851078Read ↗

Msh2 deficiency enhances somatic Apc and p53 mutations in Apc+/-Msh2-/- mice.Semantic proximity Read ↗

Myh deficiency enhances intestinal tumorigenesis in multiple intestinal neoplasia (ApcMin/+) mice.Semantic proximity Read ↗

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

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

Analysis of reciprocal congenic lines reveals the C3H/HeJ genome to be highly resistant to ApcMin intestinal tumorigenesis.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 ↗

Impact of Dnmt1 deficiency, with and without low folate diets, on tumor numbers and DNA methylation in Min mice.Semantic proximity Read ↗

Somatic mutational mechanisms involved in intestinal tumor formation in Min mice.Semantic proximity Read ↗

Tumor-associated Apc mutations in Mlh1-/- Apc1638N mice reveal a mutational signature of Mlh1 deficiency.Semantic proximity Read ↗

Suppression of intestinal and mammary neoplasia by lifetime administration of aspirin in Apc(Min/+) and Apc(Min/+), Msh2(-/-) 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 ↗

Intestinal adenomas can develop with a stable karyotype and stable microsatellitesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.