ArticleGut2005
Exon 3 beta-catenin mutations are specifically associated with colorectal carcinomas in hereditary non-polyposis colorectal cancer syndrome.
Article in Gut, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 120 citations in OpenAlex.
- Deficient mismatch repair system in patients with sporadic advanced colorectal cancer.British journal of cancer · 2009Trial
- Role of Mechanotransduction in Cancer: A Complex Problem Involving Gene Mutations and Altered Levels of Connection Components.Biomolecules · 2026Review
- Lynch Syndrome in Focus: A Multidisciplinary Review of Cancer Risk, Clinical Management, and Special Populations.Cancers · 2025Review
- A brief review of Lynch syndrome: understanding the dual cancer risk between endometrial and colorectal cancer.Oncology reviews · 2025Review
- Article
- A novel RIP1-mediated canonical WNT signaling pathway that promotes colorectal cancer metastasis via β -catenin stabilization-induced EMT.Cancer gene therapy · 2023Article
- Organoids and metastatic orthotopic mouse model for mismatch repair-deficient colorectal cancer.Frontiers in oncology · 2023Article
- Review
- Progress Report: New insights into the prevention of CRC by colonoscopic surveillance in Lynch syndrome.Familial cancer · 2022Review
- Adherens junction proteins on the move-From the membrane to the nucleus in intestinal diseases.Frontiers in cell and developmental biology · 2022Review
- Wnt/β-catenin signaling in cancers and targeted therapies.Signal transduction and targeted therapy · 2021Review
- Article
- The Canonical Wnt Signaling (Wnt/β-Catenin Pathway): A Potential Target for Cancer Prevention and Therapy.Iranian biomedical journal · 2020Review
- Cas9 Mediated Correction ofOncoTargets and therapy · 2020Article
- β-catenin activation down-regulates cell-cell junction-related genes and induces epithelial-to-mesenchymal transition in colorectal cancers.Scientific reports · 2019Article
- Excluding Lynch syndrome in a female patient with metachronous DNA mismatch repair deficient colon- and ovarian cancer.Familial cancer · 2018Article
- The role of APC in WNT pathway activation in serrated neoplasia.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018Article
- Mapping clinicopathological entities within colorectal mucinous adenocarcinomas: a hierarchical clustering approach.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- The regulation of β-catenin activity and function in cancer: therapeutic opportunities.Oncotarget · 2017Review
- Circulating Tumor DNA as Biomarkers for Cancer Detection.Genomics, proteomics & bioinformatics · 2017Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimsActivating beta-catenin mutations in exon 3 have been implicated in colorectal tumorigenesis. Although reports to the contrary exist, it has been suggested that beta-catenin mutations occur more often in microsatellite unstable (MSI+) colorectal carcinomas, including hereditary non-polyposis colorectal cancer (HNPCC), as a consequence of defective DNA mismatch repair. We have analysed 337 colorectal carcinomas and adenomas, from both sporadic cases and HNPCC families, to provide an accurate assessment of beta-catenin mutation frequency in each tumour type.
methodsDirect sequencing of exon 3 of beta-catenin.
resultsMutations were rare in sporadic (1/83, 1.2%) and HNPCC adenomas (1/37, 2.7%). Most of the sporadic adenomas analysed (80%) were small (<1 cm), and our data therefore differ from a previous report of a much higher mutation frequency in small adenomas. No oncogenic beta-catenin mutations were identified in 34 MSI+ and 78 microsatellite stable (MSI-) sporadic colorectal cancers but a raised mutation frequency (8/44, 18.2%) was found in HNPCC cancers; this frequency was significantly higher than that in HNPCC adenomas (p=0.035) and in both MSI- (p<0.0001) and MSI+ (p=0.008) sporadic cancers. Mutations were more common in higher stage (Dukes' stages C and D) cancers (p=0.001).
conclusionExon 3 beta-catenin mutations are associated specifically with malignant colorectal tumours in HNPCC; mutations appear not to result directly from deficient mismatch repair. Our data provide evidence that the genetic pathways of sporadic MSI+ and HNPCC cancers may be divergent, and indicate that mutations in the HNPCC pathway of colorectal tumorigenesis may be determined by selection, not simply by hypermutation.
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