BAC-FISH assays delineate complex chromosomal rearrangements in a case of post-Chernobyl childhood thyroid cancer

Creators: Kwan, Johnson; Baumgartner, Adolf; Lu, Chun-Mei; Wang, Mei; Weier, Jingly F.; Zitzelsberger, Horst F.; Weier, Heinz-Ulrich G.

Abstract

Structural chromosome aberrations are known hallmarks of many solid tumors. In the papillary form of thyroid cancer (PTC), for example, activation of the receptor tyrosine kinase (RTK) genes, RET and neurotrophic tyrosine kinase receptor type I (NTRK1) by intra- and interchromosomal rearrangements has been suggested as a cause of the disease. However, many phenotypically similar tumors do not carry an activated RET or NTRK-1 gene or express abnormal ret or NTRK- 1 transcripts. Thus, we hypothesize that other cellular RTK-type genes are aberrantly expressed in these tumors. Using fluorescence in situ hybridization-based methods, we are studying karyotype changes in a relatively rare subgroup of PTCs, i.e., tumors that arose in children following the 1986 nuclear accident in Chernobyl, Ukraine. Here, we report our technical developments and progress in deciphering complex chromosome aberrations in case S48TK, an aggressively growing PTC cell line, which shows an unusual high number of unbalanced translocations.

Additional Information

© 2009 Polish Histochemical et Cytochemical Society. Submitted: 10 March, 2009. Accepted after reviews: 5 May, 2009. Parts of this work have been presented at the 13th Congress of the International Federation of Societies for Histochemistry and Cytochemistry (ICHC2008), Medical University of Gdansk, Poland, August 27-30, 2008. This work was supported in parts by NIH grants CA80792, CA88258, CA123370, and HD45736, and a grant from the Director, Office of Energy Research, Office of Health and Environmental Research, U.S. Department of Energy, under contract DE-AC02-05CH11231. JFW was supported in part by NIH grant HD41425 and a grant from the UC Discovery Program, which also supported AB. Ideograms were kindly provided by D. Adler, Ph.D., Dept. of Pathology, Univ. Washington. We acknowledge the support from staff at the Helmholtz Zentrum Muenchen providing metaphase spreads and G-banding data. We also like to express our thanks to the scientists at the Human Genome Center, California Institute of Technology, Pasadena, whose generosity made these studies possible. Disclaimer: This document was prepared as an account of work sponsored by the United States Government. While this document is believed to contain correct information, neither the United States Government nor any agency thereof, nor The Regents of the University of California, nor any of their employees, makes any warranty, express or implied, or assumes any legal responsibility for the accuracy, completeness, or usefulness of any information, apparatus, product, or process disclosed, or represents that its use would not infringe privately owned rights. Reference herein to any specific commercial product, process, or service by its trade name, trademark, manufacturer, or otherwise, does not necessarily constitute or imply its endorsement, recommendation, or favoring by the United States Government or any agency thereof, or The Regents of the University of California. The views and opinions of authors expressed herein do not necessarily state or reflect those of the United States Government or any agency thereof, or The Regents of the University of California.

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