ArticleBritish journal of cancer2007
Investigation of pathogenic mechanisms in multiple colorectal adenoma patients without germline APC or MYH/MUTYH mutations.
Article in British journal of cancer, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 33 citations in OpenAlex.
- Ten or More Cumulative Lifetime Adenomas Are Associated with Increased Risk for Advanced Neoplasia and Colorectal Cancer.Digestive diseases and sciences · 2022Article
- Clinico-pathological Features of Colon Cancer Patients Undergoing Emergency Surgery: A Comparison Between Elderly and Non-elderly Patients.Open medicine (Warsaw, Poland) · 2019Article
- Familial Polyposis Coli: The Management of Desmoid Tumor Bleeding.Open medicine (Warsaw, Poland) · 2019Article
- Imaging of postoperative shoulder instability.Musculoskeletal surgery · 2017Review
- Exome Sequencing Identifies Biallelic MSH3 Germline Mutations as a Recessive Subtype of Colorectal Adenomatous Polyposis.American journal of human genetics · 2016Article
- Clinical Characteristics of Multiple Colorectal Adenoma Patients Without Germline APC or MYH Mutations.Journal of clinical gastroenterology · 2016Article
- Our experience in the treatment of Malignant Fibrous Hystiocytoma of the larynx: clinical diagnosis, therapeutic approach and review of literature.Open medicine (Warsaw, Poland) · 2016Article
- Common colorectal cancer risk alleles contribute to the multiple colorectal adenoma phenotype, but do not influence colonic polyposis in FAP.European journal of human genetics : EJHG · 2015Article
- Bowel Angiodysplasia and Myocardial Infarction secondary to an ischaemic imbalance: a case report.Open medicine (Warsaw, Poland) · 2015Article
- Colorectal cancer risk variants on 11q23 and 15q13 are associated with unexplained adenomatous polyposis.Journal of medical genetics · 2014Article
- Review
- Minimal invasive surgery in treatment of liver metastases from colorectal carcinomas: case studies and survival rates.BMC surgery · 2013Article
- Factors affecting the treatment of multiple colorectal adenomas.Surgical endoscopy · 2013Article
- Undefined familial colorectal cancer.World journal of gastrointestinal oncology · 2009Article
- Identification of susceptibility genes for cancer in a genome-wide scan: results from the colon neoplasia sibling study.American journal of human genetics · 2008Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with multiple (5-100) colorectal adenomas (MCRAs) often have no germline mutation in known predisposition genes, but probably have a genetic origin. We collected a set of 25 MCRA patients with no detectable germline mutation in APC, MYH/MUTYH or the mismatch repair genes. Extracolonic tumours were absent in these cases. No vertical transmission of the MCRA phenotype was found. Based on the precedent of MYH-associated polyposis (MAP), we searched for a mutational signature in 241 adenomatous polyps from our MCRA cases. Somatic mutation frequencies and spectra at APC, K-ras and BRAF were, however, similar to those in sporadic colorectal adenomas. Our data suggest that the genetic pathway of tumorigenesis in the MCRA patients' tumours is very similar to the classical pathway in sporadic adenomas. In sharp contrast to MAP tumours, we did not find evidence of a specific mutational signature in any individual patient or in the overall set of MCRA cases. These results suggest that hypermutation of APC does not cause our patients' disease and strongly suggests that MAP is not a paradigm for the remaining MCRA patients. Our MCRA patients' colons showed no evidence of microadenomas, unlike in MAP and familial adenomatous polyposis (FAP). However, nuclear beta-catenin expression was significantly greater in MCRA patients' tumours than in sporadic adenomas. We suggest that, at least in some cases, the MCRA phenotype results from germline variation that acts subsequent to tumour initiation, perhaps by causing more rapid or more likely progression from microadenoma to macroadenoma.
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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.