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Carcinogenesis, Vol. 23, No. 10, 1577-1582, October 2002
© 2002 Oxford University Press

CANCER BIOLOGY

Differential mutation frequency in mitochondrial DNA from thyroid tumours

H.D. Lohrer1,2,3, L. Hieber2 and H. Zitzelsberger2

1 Radiobiological Institute, University of Munich, Schillerstrasse 42, D-80336 Munich, Germany and
2 Institute of Molecular Radiation Biology, GSF—National Research Centre for Environment and Health, Ingolstädter Landstrasse 1, D-85764 Neuherberg, Germany

Lack of a chromatin structure and histone protection makes mitochondrial DNA susceptible to oxidative damage. Suboptimal DNA repair leads to a higher frequency of mitochondrial mutations, which are associated with aging, carcinogenesis and environmental insult. The instability of the hypervariable region II of the mitochondrial genome was investigated in radiation-associated thyroid tumours, which were diagnosed in children from Belarus after the accident at the Chernobyl nuclear power plant, and from 40 sporadic thyroid tumours from Munich. Two mutations were identified in two out of 126 tumours from Belarus, and eight mutations were found in six out of 40 tumours from Munich. All mutations were deletions or insertions of C in a poly-cytidine (C7TC6) microsatellite. The mutation frequency correlated with the age of the patients at surgery. Mutations with the typical pattern of base substitutions following oxidative DNA damage were not identified.


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