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Cytogenetic Changes in Radiation-induced Tumors of the Thyroid¹

Institute of Radiobiology, GSF-Forschungszentrum für Umwelt und Gesundheit GmbH, D-85764 Neuherberg, Germany [H. Z., L. L., L. H., T. N., K. S., A. M. K., M. B.]; Life Sciences Division, E. O. Lawrence Berkeley National Laboratory, Berkeley, California 94720 [H-U. G. W., J. F.]; Applied Spectral Imaging, Inc., Carlsbad, California 92009 [C. J.]; Reproductive Genetics Unit, Department of Obstetrics, Gynecology, and Reproductive Sciences, University of California, San Francisco, California 94143 [J. F.]; Martha-Maria Krankenhaus, München, Germany [F. S.]; Center for Thyroid Tumors, 220600 Minsk, Belarus [E. P. D.]; Institut für Pathologie und Pathologische Anatomie, Technische Universität München, D-84675 Munich, Germany [M. W.]; and Institute of Radiation Biology, Ludwig Maximilians University, D-80336 München, Germany [H. Z., E. L., A. M. K.]

Thyroid carcinoma incidence is increased significantly after ionizing irradiation; however, the possible mechanisms have not yet been identified. To provide clues for an understanding of the radiation-induced transformation of thyroid epithelium, we analyzed the karyotypes of 56 childhood thyroid tumors that appeared in Belarus after the Chernobyl nuclear accident in 1986. We also studied eight secondary thyroid tumors that developed after radiotherapy. Metaphase preparations obtained from primary cultures were analyzed by G-banding. Clonal structural aberrations were found in 13 of 56 Belarussian cases and in 6 of 8 secondary tumors that developed after radiotherapy. Furthermore, we detected multiple chromosomal aberrations as well as complex rearrangements in some of these tumors and performed a detailed analysis of marker chromosomes from a single case using spectral karyotyping and comparative genomic hybridization in a childhood tumor from Belarus with a near-triploid karyotype. Both comparative genomic hybridization and spectral karyotyping analysis revealed structural alterations affecting identical chromosomes 1, 2, 9, and 13, among others. In addition to the known hot spots of alterations in papillary thyroid carcinomas on chromosomes 1q and 10q, a comprehensive breakpoint analysis in the pooled data set revealed novel breakpoints on chromosomes 4q, 5q, 6p, 12q, 13q, and 14q. The chromosomal aberrations in these tumors may provide suitable starting points for the positional cloning of genes involved in radiation-induced tumorigenesis.

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