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Research Article Free access | 10.1172/JCI115232

Rearrangements of the tal-1 locus as clonal markers for T cell acute lymphoblastic leukemia.

O G Jonsson, R L Kitchens, R J Baer, G R Buchanan, and R G Smith

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Jonsson, O. in: PubMed | Google Scholar

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Kitchens, R. in: PubMed | Google Scholar

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Baer, R. in: PubMed | Google Scholar

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Buchanan, G. in: PubMed | Google Scholar

Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas 75235.

Find articles by Smith, R. in: PubMed | Google Scholar

Published June 1, 1991 - More info

Published in Volume 87, Issue 6 on June 1, 1991
J Clin Invest. 1991;87(6):2029–2035. https://doi.org/10.1172/JCI115232.
© 1991 The American Society for Clinical Investigation
Published June 1, 1991 - Version history
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Abstract

Normal and aberrant immune receptor gene assembly each produce site-specific DNA rearrangements in leukemic lymphoblasts. In either case, these rearrangements provide useful clonal markers for the leukemias in question. In the t(1;14)(p34;q11) translocation associated with T cell acute lymphoblastic leukemia (T-ALL), the breakpoints on chromosome 1 interrupt the tal-1 gene. A site-specific deletion interrupts the same gene in an additional 26% of T-ALL. Thus, nearly one-third of these leukemias contain clustered rearrangements of the tal-1 locus. To test whether these rearrangements can serve as markers for residual disease, we monitored four patients with T-ALL; three of the leukemias contained a deleted (tald) and one a translocated (talt) tal-1 allele. These alleles were recognized by a sensitive amplification/hybridization assay. tald alleles were found in the blood of one patient during the 4th mo of treatment but not thereafter. Using a quantitative assay to measure the fraction of tald alleles in DNA extracts, we estimated that this month 4 sample contained 150 tald copies per 10(6) genome copies. The patient with t(1;14)(p34;q11) (talt) leukemia developed a positive assay during the 20th mo of treatment. By standard criteria, all four patients remain in complete remission 11-20 mo into treatment. We conclude that tal-1 rearrangements provide useful clonal markers for approximately 30% of T-ALLs.

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