ArticleBMC cancer2005
Mutations in APC, CTNNB1 and K-ras genes and expression of hMLH1 in sporadic colorectal carcinomas from the Netherlands Cohort Study.
Article in BMC cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 68 citations in OpenAlex.
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- FIBP knockdown attenuates growth and enhances chemotherapy in colorectal cancer via regulating GSK3β-related pathways.Oncogenesis · 2018Article
- Molecular regulation and pharmacological targeting of the β-catenin destruction complex.British journal of pharmacology · 2017Review
- Progression inference for somatic mutations in cancer.Heliyon · 2017Article
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- Scientific Evidence of Rice By-Products for Cancer Prevention: Chemopreventive Properties of Waste Products from Rice Milling on CarcinogenesisBioMed research international · 2017Review
- Molecular spectrum ofJournal of gastrointestinal oncology · 2016Article
- Targeted molecular profiling of rare genetic alterations in colorectal cancer using next-generation sequencing.Medical oncology (Northwood, London, England) · 2016Article
- Wnt-signalling pathways and microRNAs network in carcinogenesis: experimental and bioinformatics approaches.Molecular cancer · 2016Review
- A unique profile of adenomatous polyposis coli gene mutations in Iranian patients suffering sporadic colorectal cancer.Cell journal · 2014Article
- Expression of the mismatch repair gene hMLH1 is enhanced in non-small cell lung cancer with EGFR mutations.PloS one · 2013Article
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- Comparison of beta-catenin with TGF-beta1, HIF-1alpha and patients' disease-free survival in human colorectal cancer.Pathology oncology research : POR · 2010Article
- Involvement of oxidatively damaged DNA and repair in cancer development and aging.American journal of translational research · 2010Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe early to intermediate stages of the majority of colorectal tumours are thought to be driven by aberrations in the Wnt (APC, CTNNB1) and Ras (K-ras) pathways. A smaller proportion of cancers shows mismatch repair deficiency. The aim of this study was to analyse the co-occurrence of these genetic alterations in relation to tumour and patient characteristics.
methodsIn a group of 656 unselected sporadic colorectal cancer patients, aberrations in the APC, K-ras, CTNNB1 genes, and expression of hMLH1 were investigated. Additionally, tumours were divided in groups based on molecular features and compared with respect to patient's age at diagnosis, sex, family history of colorectal cancer, tumour sub-localisation, Dukes' stage and differentiation.
resultsMutations at the phosphorylation sites (codons 31, 33, 37, and 45) in the CTNNB1 gene were observed in tumours from only 5/464 patients. Tumours with truncating APC mutations and activating K-ras mutations in codons 12 and 13 occurred at similar frequencies (37% (245/656) and 36% (235/656), respectively). Seventeen percent of tumours harboured both an APC and a K-ras mutation (109/656). Nine percent of all tumours (58/656) lacked hMLH1 expression. Patients harbouring a tumour with absent hMLH1 expression were older, more often women, more often had proximal colon tumours that showed poorer differentiation when compared to patients harbouring tumours with an APC and/or K-ras mutation.
conclusionCTNNB1 mutations seem to be of minor importance in sporadic colorectal cancer. The main differences in tumour and patient characteristics are found between groups of patients based on mismatch repair deficiency.
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