Microsatellite instability: new aspects in the carcinogenesis of colorectal carcinoma

Very recently a new molecular mechanism in the tumorigenesis of colorectal carcinoma has been described which is closely linked to hereditary non-polyposis colonic cancer (HNPCC). Ubiquitous changes in the length of simple repetitive DNA sequences between constitutional and tumour DNA occur in about...

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Bibliographic Details
Published in:Virchows Archiv : an international journal of pathology 1995-04, Vol.426 (3), p.215-222
Main Authors: RÜSCHOFF, J, BOCKER, T, SCHLEGEL, J, STUMM, G, HOFSTAEDTER, F
Format: Article
Language:English
Subjects:
Biological and medical sciences
Carcinogens - pharmacology
Carcinoma - congenital
Carcinoma - etiology
Carcinoma - genetics
Colorectal Neoplasms - congenital
Colorectal Neoplasms - etiology
Colorectal Neoplasms - genetics
DNA Repair - genetics
DNA Repair - physiology
DNA, Satellite - genetics
Female
Gastroenterology. Liver. Pancreas. Abdomen
Humans
Male
Medical sciences
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Tumors
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Summary:Very recently a new molecular mechanism in the tumorigenesis of colorectal carcinoma has been described which is closely linked to hereditary non-polyposis colonic cancer (HNPCC). Ubiquitous changes in the length of simple repetitive DNA sequences between constitutional and tumour DNA occur in about 90% of cases of HNPCC and in about 15% of cases of non-familial, sporadic colorectal carcinoma. Such microsatellite instabilities have been shown to be the phenotypical marker of mutations in the human homologues of prokaryotic mismatch repair genes (MutS, MutL, MutH). These data provide crucial new tools in the detection of patients at high risk of developing colon cancer and other HNPCC-related carcinomas. In addition, these developments provide new insights into a new, presumably primary event in oncogenesis, i.e. the occurrence of mutations in genomic stability genes leading to an increased cellular mutation rate ("mutator phenotype") and thus to cancer.
ISSN:0945-6317
1432-2307
DOI:10.1007/BF00191357