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PMID: 2303782 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

The chromosome translocation (11;14)(p13;q11) associated with T cell acute leukemia. Asymmetric diversification of the translocational junctions.

The Journal of experimental medicine ·Vol. 171 ·No. 2 ·1990-02-01 ·Pages 489-501

Cheng JT, Yang CY, Hernandez J, Embrey J, Baer R

Abstract

The t(11;14)(p13;q13) translocation associated with T cell acute lymphocytic leukemia generates two abnormal chromosomes, designated 11p+ and 14q-. To investigate the mechanism of t(11;14)(p13;q11) formation, we analyzed the translocation junctions of 11p+ and 14q- from two patients. The 11p+ junctions consisted of precise fusions of a pseudo recombination signal from chromosome 11 and the downstream recombination signal of the TCR D delta 2 gene segment from chromosome 14. In contrast, the 14q- junctions from both patients were diversified by random loss and addition of nucleotides at the translocation site. This asymmetric pattern of junctional diversification is typical of normal Ig/TCR gene rearrangement, and therefore implies that the t(11;14)(p13;q11) translocation arose due to aberrant activity of the Ig/TCR recombinase.

MeSH Terms
Adult Base Sequence Blotting, Southern Child, Preschool Chromosomes, Human, Pair 11 Chromosomes, Human, Pair 14 Gene Rearrangement, T-Lymphocyte Humans Leukemia-Lymphoma, Adult T-Cell/genetics Male Molecular Sequence Data Polymerase Chain Reaction Translocation, Genetic
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Cheng J T
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas 75235.
Yang C Y
Hernandez J
Embrey J
Baer R
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Article Info
Journal
The Journal of experimental medicine
Abbr.
J Exp Med
ISSN
0022-1007
Published
1990-02-01
Pages
489-501
Language
English
Region
United States
NLM ID
2985109R
PMCID
PMC2187731
Subset
IM
Grants
NCI NIH HHS · CA-46593 · United States
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