Carcinogenesis, Vol. 20, No. 12, 2247-2252,
December 1999
© 1999 Oxford University Press
Cancer Biology |
Microsatellite instability and loss of heterozygosity in radiation-associated thyroid carcinomas of Belarussian children and adults
1 Radiobiological Institute, University of Munich (LMU), Schillerstraße 42, 80336 Munich, Germany and
2 Institute of Radiobiology, GSF-National Research Center for Environment and Health, Ingolstaedter Landstrasse 1, 85758 Neuherberg, Germany
DNA from 129 paired thyroid tumorous and non-tumorous tissue samples of Belarussian children (102 patients; age at surgery 
18 years) and adults (27 patients; age at surgery 19–35 years), who had been exposed to radioactive fallout from the Chernobyl reactor accident in 1986, was examined for microsatellite instability (MSI) and loss of heterozygosity (LOH). Twenty-eight microsatellite markers were chosen because of their vicinity to DNA repair genes or genes involved in tumorigenesis as well as regions of chromosomal breakpoints in thyroid tumours. In 40 patients (31% of 129) we detected a total of 73 alterations, 80% of which were classified as LOH and only 20% as MSI. Amongst these 40 patients we identified a subgroup of 11, mainly young female patients (8.5% of 129), exhibiting alterations in at least two microsatellite markers. For comparison we examined samples from spontaneous thyroid carcinomas without radiation history from 20 adult patients from Munich (mean age at surgery 56 ± 13 years). None of the tumour samples investigated showed evidence of alterations in the 28 microsatellite markers tested. Taken together our data indicate an increased instability of microsatellite markers in thyroid cancers from Belarussian patients. At present, it is uncertain whether the increased genome instability observed in Belarussian patients is the result of the exposure to radioactive iodine from the Chernobyl reactor accident or due to the young age of the patients.
Abbreviations: APC, adenomatous polyposis coli; BRCA1/BRCA2, breast cancer genes 1 and 2; DCC, deleted colorectal cancer; FES, feline sarcoma; hMLH1, human MutL-homolog 1; HNPCC, hereditary non-polyposis colorectal cancer; HPRT, hypoxanthine phosphoribosyltransferase; LOH, loss of heterozygosity; MSI, microsatellite instability; MYC, avian myelocytomatosis; RET, receptor-typ tyrosine kinase; RETINT5, receptor-typ tyrosine kinase, intron V; XRCC1 and XRCC5, X-ray repair cross complementing 1 and 5.
3 To whom correspondence should be addressed Email: richter{at}gsf.de
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