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Case Reports
. 1989 Jan;86(2):602-6.
doi: 10.1073/pnas.86.2.602.

Molecular analysis of a t(14;14) translocation in leukemic T-cells of an ataxia telangiectasia patient

G Russo  1 , M Isobe, R Gatti, J Finan, O Batuman, K Huebner, P C Nowell, C M Croce
Affiliations
Case Reports

Molecular analysis of a t(14;14) translocation in leukemic T-cells of an ataxia telangiectasia patient

G Russo et al. Proc Natl Acad Sci U S A. 1989 Jan.

Abstract

We have detected and cloned two rearrangements in the T-cell receptor alpha locus from a clone of somatic cell hybrids carrying a t(14;14)(q11;q32) chromosomal translocation derived from an ataxia telangiectasia patient with T-cell chronic lymphocytic leukemia. The T-cell clone carrying the t(14;14) chromosomal translocation was known to be present for greater than 10 years before the onset of overt leukemia. One molecular rearrangement of the T-cell receptor alpha locus corresponded to a functional variable-joining region (V-J) joining, whereas the other derived from the breakpoint of the t(14;14)(q11;q32) translocation. Chromosomal in situ hybridization of the probe derived from the t(14;14) breakpoint localized the breakpoint region to 14q32.1, apparently the same region that is involved in another ataxia telangiectasia characteristic chromosome translocation, t(7;14)(q35;q32). The 14q32.1 breakpoint is at least 10,000 kilobase pairs (kbp) centromeric to the immunoglobulin heavy chain locus. Sequence analysis of the breakpoint indicates the involvement of a J alpha sequence during the translocation. Comigration of high-molecular weight DNA fragments involved with t(7;14) and t(14;14) translocations suggests the presence of a cluster of breakpoints in the 14q32.1 region, the site of a putative oncogene, TCL1.

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