Affiliations: Institute of Pathology, Johannes Gutenberg-University of Mainz, Langenbeckstr. 1, 55101 Mainz, Germany | Laboratory of Pathology, Gene Regulation Section, National Cancer Institute, NIH, Bethesda 20892, MD, USA | King Faisal Specialist Hospital & Research Centre, Children's Cancer Centre, PO Box 3354, MBC # 98-16, Riyadh 11211, Saudi Arabia
Note: [] Corresponding author: Dr. Achim Weber, Institute of Pathology, Johannes Gutenberg-University of Mainz, Langenbeckstr. 1, 55101 Mainz, Germany. Tel.: +49 6131 174201; Fax: +49 6131 17474201; E-mail: [email protected].
Abstract: Background: Chromosomal translocations are causally related to the development of many tumors. In Burkitt's lymphoma, abnormalities involving the c-myc gene are essential. The CT-element of the c-myc promoter adopts non-B-conformation in vivo and in vitro, and therefore provides a potential fragile site. Methods: We have developed a LM-PCR-based approach to test if chromosomal breakpoints indeed cluster in this region. Results: Amplifying both, wild-type as well as the translocated c-myc gene by LM-PCR, it was shown that chromosomal breakpoints did not cluster within the CT-element. Conclusions: Therefore, the CT-element is not especially susceptible to the formation of breakpoints leading to chromosomal translocations in Burkitt's lymphoma.
