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A frequent site of translocation damage in human T-ALL has been localized to a specific region of chromosome band 11p13. Five new T-ALL cases are described which break in the major T-ALLbcr region of 11p13, two involving a novel translocation t(7;11)(q35;p13), with breakage at the T cell receptor (TCR) beta gene from 7q35, and three involving TCR delta from 14q11 in the more common t(11;14)(p13;q11). Analysis of the mechanism of one T-ALLbcr/TCR beta translocation and a previously described t(11;14)(p13;q11) was conducted by genomic cloning of translocation breakpoints, using the polymerase chain reaction (PCR). Both seem to have occurred by recombinase error, but only the t(7;11) showed sequence-specific joining. Nonetheless recombinase mediation of the t(11;14) is implied by the presence of N-region addition (a hallmark of recombinase joins) on both derivative chromosomes. These observations reinforce the view that translocations in the T-ALLbcr region of chromosome 11p13 are a major lesion in human T-ALL. In addition, these can occur by mimicry of VDJ joining, but sequence specificity is not obligatory.


Journal article



Publication Date





577 - 582


Base Sequence, Chromosome Deletion, Chromosomes, Human, Pair 11, Chromosomes, Human, Pair 7, Cloning, Molecular, Humans, Leukemia-Lymphoma, Adult T-Cell, Molecular Sequence Data, Polymerase Chain Reaction, Receptors, Antigen, T-Cell, Receptors, Antigen, T-Cell, alpha-beta, Receptors, Antigen, T-Cell, gamma-delta, Restriction Mapping, Translocation, Genetic