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Article

The 'just-right' signaling model: APC somatic mutations are selected based on a specific level of activation of the beta-catenin signaling cascade.

Human molecular genetics - 15 Jun 2002

Albuquerque Cristina, Breukel Cor, van der Luijt Rob, Fidalgo Paulo, Lage Pedro, Slors Frederik J M, Leitão C Nobre, Fodde Riccardo, Smits Ron

Abstract excerpt

According to the classical interpretation of Knudson's 'two-hit' hypothesis for tumorigenesis, the two 'hits' are independent mutation events, the end result of which is loss of a tumor suppressing function. Recently, it has been shown that the APC (adenomatous polyposis coli) gene does not entirely follow this model. Both the position and type of the second hit in familial adenomatous polyposis (FAP) polyps...

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Share to Adenomatous Polyposis Coli
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Chromosomes, Human, Pair 10

Share to Chromosomes, Human, Pair 5

Share to Loss of Heterozygosity

Share to Repetitive Sequences, Amino Acid

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Source

Identifiers

PMID: 12045208
DOI: 10.1093/hmg/11.13.1549

Genes

APC
FAP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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The 'just-right' signaling model: APC somatic mutations are selected based on a specific level of activation of the beta-catenin signaling cascade.PMID 12045208Read ↗

The type of somatic mutation at APC in familial adenomatous polyposis is determined by the site of the germline mutation: a new facet to Knudson's 'two-hit' hypothesis.Semantic proximity Read ↗

The APC Variant p.Glu1317Gln predisposes to colorectal adenomas by a novel mechanism of relaxing the target for tumorigenic somatic APC mutations.Semantic proximity Read ↗

Refining the relation between 'first hits' and 'second hits' at the APC locus: the 'loose fit' model and evidence for differences in somatic mutation spectra among patients.Semantic proximity Read ↗

APC and the three-hit hypothesis.Semantic proximity Read ↗

APC mutations in FAP-associated desmoid tumours are non-random but not 'just right'.Semantic proximity Read ↗

APC mutations in sporadic colorectal tumors: A mutational "hotspot" and interdependence of the "two hits".Semantic proximity Read ↗

Disease severity and genetic pathways in attenuated familial adenomatous polyposis vary greatly but depend on the site of the germline mutation.Semantic proximity Read ↗

Different APC genotypes in proximal and distal sporadic colorectal cancers suggest distinct WNT/β-catenin signalling thresholds for tumourigenesis.Semantic proximity Read ↗

Quantifying ‘just-right’ APC inactivation for colorectal cancer initiationSemantic proximity Read ↗

The Apc 1322T mouse develops severe polyposis associated with submaximal nuclear beta-catenin expression.Semantic proximity Read ↗

Different combinations of biallelic APC mutation confer different growth advantages in colorectal tumours.Semantic proximity Read ↗

Loss of beta-catenin regulation by the APC tumor suppressor protein correlates with loss of structure due to common somatic mutations of the gene.Semantic proximity Read ↗

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