Jumping translocations of 11q in acute myeloid leukemia and 1q in follicular lymphoma

Jumping translocation is a rare cytogenetic aberration in leukemia and lymp homa, and its etiologic mechanisms are not clearly known. We report two cas es with jumping translocations. One had follicular lymphoma and jumping tra nslocations of Iq onto the telomeric regions of 5p, 9p, and 15q in three ce ll lines, co-existing with the specific translocation t(14;18)(q32;q21). Th e second case had acute myeloid leukemia (AML) and jumping translocations o f 11q as the sole aberration, onto multiple derivative chromosomes in each of the abnormal cells. A total of 17 telomeric regions were seen as the rec ipients of 11q in this case, and 9q was always involved as one of the recip ients in all abnormal cells. Fluorescence in situ hybridization (FISH) conf irmed the identification of 11q material in the derivative chromosomes. Whi le Iq has been the most common donor of acquired jumping translocations, th is is the first report on jumping translocations of 11q. Different from all previously reported jumping translocations which involve only one recipien t in each cell line and lead to a mosaic trisomy multiple recipients in mos t of the abnormal cells in this case had led to a tetrasomy, or a pentasomy of 11q. The pattern of chromosome involvement as the recipients of 11q app ears to show a continuing evolutionary process of jumping, stabilization, a nd spreading of the donor material into other chromosomes. Somatic recombin ations between the interstitial telomeric or subtelomeric sequences of a de rivative chromosome and the telomeric sequences of normal chromosomes are b elieved to be the underlying mechanism of jumping translocations and their clonal evolution. (C) Elsevier Science Inc., 2000. All rights reserved.