Heterogeneity of breakpoints at the transcriptional co-activator gene, BOB-1, in lymphoproliferative disease

• Published in: Leukemia Vol. 10; no. 9; p. 1492
• Main Authors: Yuille, M A, Galiegue-Zouitina, S, Hiorns, L R, Jadayel, D, De Schouwer, P J, Catovsky, D, Dyer, M J, Kerckaert, J P
• Format: Journal Article
• Language: English
• Published: England 01.09.1996
• Subjects: Base Sequence; Chromosomes, Human, Pair 11; DNA Probes; DNA, Neoplasm - genetics; Exons; Gene Rearrangement; Humans; In Situ Hybridization, Fluorescence; Karyotyping; Leukemia, Prolymphocytic - genetics; Leukemia-Lymphoma, Adult T-Cell - genetics; Lymphoproliferative Disorders - genetics; Molecular Sequence Data; Trans-Activators - genetics; Tumor Cells, Cultured
• ISSN: 0887-6924; 1476-5551

Chromosome 11q23 is frequently a site of chromosomal translocation in both acute leukemias and chronic lymphoproliferative disorders. In the former, an 8 kb region within the MLL gene is consistently involved, whereas in the latter breakpoints appear to be heterogeneous. In a B cell acute leukemia cell line with t(14;18)(q32.3;q21.3) we have previously demonstrated a reciprocal translocation between the LAZ3/BCL6 gene at 3q27 and the B cell specific transcriptional coactivator gene BOB-1 at 11q23.1, implicating BOB-1 as a potential proto-oncogene. To confirm the chromosomal localization of BOB-1 we have mapped it by FISH to 11q23.1. It lay immediately telomeric of the ATM gene. We have also investigated the frequency of BOB-1 rearrangements in a panel of 32 cell lines and 71 patient samples. In one case of T cell prolymphocytic leukemia-a disease where 11q23 abnormalities are observed-a chromosomal rearrangement was identified 3.3-0.9 kb centromeric of the 3' end of the gene. Thus, there is a heterogeneity of breakpoints associated with BOB-1 while the frequency of the gene's involvement in lymphoproliferative diseases is low.