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

Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas.

The Journal of pathology - 1 May 2010

Obrador-Hevia Antònia, Chin Suet-Feung, González Sara, Rees Jonathan, Vilardell Felip, Greenson Joel K, Cordero David, Moreno Víctor, Caldas Carlos, Capellá Gabriel

Abstract excerpt

Recent studies have suggested that APC loss alone may be insufficient to promote aberrant Wnt/beta-catenin signalling. Our aim was to comprehensively characterize Wnt signalling components in a set of APC-associated familial adenomatous polyposis (FAP) tumours. Sixty adenomas from six FAP patients with known pathogenic APC mutations were included. Somatic APC and KRAS mutations, beta-catenin immunostaining, and...

Read the complete abstract on PubMed

Topics

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

Share to Adenomatous Polyposis Coli
Share to Adenomatous Polyposis Coli Protein

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to beta Catenin

Share to Comparative Genomic Hybridization

Share to Genes, APC

Share to Loss of Heterozygosity

Share to ras Proteins

Share to Wnt Proteins

Source

Identifiers

PMID: 20196079
DOI: 10.1002/path.2685

Genes

APC
FAP
KRAS
MYC
AXIN2
SFRP1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Oncogenic KRAS is not necessary for Wnt signalling activation in APC-associated FAP adenomas.PMID 20196079Read ↗

Somatic Mutations in Familial Adenomatous PolypsSemantic proximity Read ↗

Somatic mutations in familial adenomatous polyps. Nuclear translocation of beta-catenin requires more than biallelic APC inactivation.Semantic proximity Read ↗

Molecular drivers of tumor progression in microsatellite stable APC mutation-negative colorectal cancers.Semantic proximity Read ↗

Promoter hypermethylation leads to decreased APC mRNA expression in familial polyposis and sporadic colorectal tumours, but does not substitute for truncating mutations.Semantic proximity Read ↗

Singapore familial adenomatous polyposis (FAP) patients with classical adenomatous polyposis but undetectable APC mutations have accelerated cancer progression.Semantic proximity Read ↗

Colorectal cancer and genetic alterations in the Wnt pathway.Semantic proximity Read ↗

Inactivation of the<i>APC</i>Gene Is Constant in Adrenocortical Tumors from Patients with Familial Adenomatous Polyposis but Not Frequent in Sporadic Adrenocortical CancersSemantic proximity Read ↗

Comprehensive mutation analysis in colorectal flat adenomas.Semantic proximity Read ↗

Analysis of K-ras, APC, and beta-catenin in aberrant crypt foci in sporadic adenoma, cancer, and familial adenomatous polyposis.Semantic proximity Read ↗

Identification of somatic APC gene mutations in periampullary adenomas in a patient with familial adenomatous polyposis (FAP).Semantic proximity Read ↗

The effect of a germline mutation in the APC gene on β-catenin in human embryonic stem cells.Semantic proximity Read ↗

Familial adenomatous polyposis (FAP) and its gene, APC.Semantic proximity Read ↗

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