Site-specific recombination of the tal-1 gene is a common occurrence in human T cell leukemia

Lamorna Brown, Jiin Tsuey Cheng, Qi Chen, Michael J. Siciliano, William Crist, George Buchanan, Richard Baer

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339 Scopus citations


The tal-1 gene is altered as a consequence of the t(1;14) (p32;q11) chromosome translocation observed in 3% of patients with T cell acute lymphoblastic leukemia (T-ALL). tal-1 encodes a helix-loop-helix (HLH) domain, a DNA binding and dimerization motif found in a number of proteins involved in cell growth and differentiation. We now report that an additional 25% of T-ALL patients bear tal-1 gene rearrangements that are not detected by karyotype analysis. These rearrangements result from a precise 90 kb deletion (designated tald) that arises independently in different patients by site-specific DNA recombination. Since the deletion junctions resemble the coding joints of assembled immunoglobulin genes, tald rearrangements are likely to be mediated by aberrant activity of the immunoglobulin recombinase. Moreover, t(1;14)(p32;q11) translocations and tald rearrangements disrupt the coding potential of tal-1 in an equivalent manner, and thereby generate a common genetic lesion shared by a significant proportion of T-ALL patients.

Original languageEnglish (US)
Pages (from-to)3343-3351
Number of pages9
JournalEMBO Journal
Issue number10
StatePublished - 1990


  • Gene rearrangement
  • Human
  • Site-specific recombination
  • Tal-1/T cell leukemia

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • General Immunology and Microbiology
  • Molecular Biology
  • General Neuroscience


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