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c-tal, a helix-loop-helix protein, is juxtaposed to the T-cell receptor-
beta chain gene by a reciprocal chromosomal translocation: t(1;7)(p32;q35)
TJ Fitzgerald, GA Neale, SC Raimondi and RM Goorha
Department of Virology and Molecular Biology, St Jude Children's Research
Hospital, Memphis, TN 38101.
Studies on nonrandom chromosomal translocations have been important for the
identification of genes potentially involved in the malignant
transformation of cells. The most widely studied translocations, involving
members of the Ig supergene family, have shown juxtapositions of
proto-oncogenes with the rearranging loci. Such translocations can
inappropriately activate expression of the proto-oncogenes and thereby play
a role in tumorigenesis. Because the cytogenetic analysis of a bone marrow
sample from a child with T-cell acute lymphoblastic leukemia showed a
(1;7)(p32;q35) translocation, we sought to determine if the translocation
breakpoint was in the T-cell receptor (TCR)-beta gene locus on chromosome
7. Analysis of the TCR-beta gene by Southern blotting showed three
rearranged bands. Nucleotide sequencing and Southern blot analysis of
TCR-beta genomic clones, isolated from patient DNA, showed that one
contained a normal rearrangement of the TCR-beta gene using V beta 12.2, D
beta 2.1, and J beta 2.5, whereas two other clones contained DNA from
derivative chromosomes 1 and 7. Chromosomal mapping showed that the (1;7)
translocation breakpoint was 35 kb 3' to the c-tal gene locus. The
juxtaposition of c-tal to the TCR- beta locus may enhance c-tal expression
and contribute to T-cell leukemogenesis.
Volume 78,
Issue 10,
pp. 2686-2695,
11/15/1991
Copyright © 1991 by The American Society of Hematology
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