ReviewOncogene2006
Colorectal cancer and genetic alterations in the Wnt pathway.
Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
298 citing papers in PubMed, 1 synthesis or guideline pooled it, 582 citations in OpenAlex.
- Aberrant promoter methylation of the vimentin gene may contribute to colorectal carcinogenesis: a meta-analysis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Pooled it
- Focus on 16p13.3 Locus in Colon Cancer.PloS one · 2015Trial
- Paracrine activation of WNT/β-catenin pathway in uterine leiomyoma stem cells promotes tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2013Trial
- Colorectal cancer molecular subtypes and prognostic models based on NET-related genes and oxidative stress-associated signaling.Medicine · 2026Article
- Metastatic colorectal adenocarcinoma with APC and EGFR L858R co-mutations: a case report.The oncologist · 2026Article
- Acromegaly and colorectal cancer risk: emerging roles of the gut microbiota.Frontiers in endocrinology · 2026Review
- Mathematical Modeling Quantifies "Just-Right" APC Inactivation for Colorectal Cancer Initiation.Cancer research · 2025Article
- A pathway-informed mutual exclusivity framework to detect genetic interactions in pediatric cancer.BMC medical genomics · 2025Article
- Innovative horizons: harnessing drug repositioning for targeted therapeutics in colorectal cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Targeted protein degradation of Wnt/β-catenin signaling pathway: an effective strategy for cancer therapy.Journal of translational medicine · 2025Review
- Genetic variants linked to type 2 diabetes in CDKN1B and TCF7L2 influence survival outcomes in metastatic colorectal cancer.International journal of cancer · 2025Article
- Evolutionary conservation and cancer implications of the WNT signaling pathway.Medical oncology (Northwood, London, England) · 2025Review
- A Haplotype GWAS in Syndromic Familial Colorectal Cancer.International journal of molecular sciences · 2025Article
- Colorectal cancer as a complex adaptive system: integrating the hallmarks of cancer with complexity theory.Frontiers in oncology · 2025Article
- Article
- Investigating the WNT and TGF-beta pathways alterations and tumor mutant burden in young-onset colorectal cancer.Scientific reports · 2024Article
- The Histogenetic Origin of Malignant Cells Predicts Their Susceptibility towards Synthetic Lethality Utilizing theCancers · 2024Article
- Interactions between genistein and Wnt pathway in colon adenocarcinoma and early embryos.Heliyon · 2024Article
- Article
- Incidences of colorectal adenomas and cancers under colonoscopy surveillance suggest an accelerated "Big Bang" pathway to CRC in three of the four Lynch syndromes.Hereditary cancer in clinical practice · 2024Article
238 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In colorectal tumours, Wnt pathway genetics continues to be dominated by mutations in the adenomatous polyposis coli (APC) gene. Germline mutations cause familial adenomatous polyposis and at least two-thirds of sporadic colorectal tumours also acquire APC mutations, quite possibly as the initiating events in tumorigenesis. These mutations almost always cause loss of the C-terminal functions of the APC protein - probably involved in microtubule binding, cell polarity and chromosome segregation - and deletion of the SAMP repeats that are important for binding to axin and formation of the beta-catenin phosphorylation complex. The truncated APC proteins are, in general, stable and almost certainly retain some activity in beta-catenin binding. The 'two hits' at APC are coselected so as to produce an optimal activation of Wnt signalling (just-right hypothesis). In a minority of colorectal tumours, Wnt activation can occur through mutations that affect phosphorylation sites within exon 3 of beta-catenin, causing protein stabilization. In other tumours, epigenetic transcriptional silencing or mutation of the secreted frizzled-related proteins may modulate Wnt levels. Mutations in the Wnt components AXIN1, AXIN2 and TCF4 have been found in microsatellite-unstable colon cancers, but it is not clear in every case whether these changes are functional. Therapeutic modulation of the Wnt pathway remains an attractive therapeutic possibility for colorectal carcinomas.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.