Non-random jumping translocations as a result of SV40 large T-antigen expression in benign human tumor cells.
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 1995 International Federation for Cell Biology
Cell Biology International
Volume 19, Issue 4, pages 315–322, April 1995
How to Cite
Kazmierczak, B., Stern, C., Bartnitzke, S. and Bullerdiek, J. (1995), Non-random jumping translocations as a result of SV40 large T-antigen expression in benign human tumor cells. Cell Biology International, 19: 315–322. doi: 10.1006/cbir.1995.1074
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
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In an attempt to analyse the cytogenetic effects caused by SV40 large T-antigen expression in cells of human benign tumors we transfected cells of an uterine leiomyoma characterized by a primary reciprocal translocation t(12;14)(q15;q24) and a pleomorphic adenoma of the salivary gland with an inversion inv(12) (q15q24.1) using a construct coding for SV40 large and small T-antigen. The most interesting finding was not a generally destabilized karyotype, but the strictly non-random involvement of two chromosomal breakpoints, i.e. 5p13 and 10q11 in jumping translocations, never described before as a result of SV40 transformation. In addition we were able to show by non-radioactive in situ hybridization that there was no direct relationship between the integration site of the construct and the pre-disposition of 5p13 and 10q11 to somatic recombination. The jumping translocations with consistent breakpoints observed closely resemble the cytogenetic situation seen in a variety of human tumors with specific translocations. Based on the findings described here it is tempting to assume that the expression of SV40 large T-antigen can induce specific karyotypic alterations following an unknown trans-acting mechanism.