Juxtaposition of the T-cell receptor α-chain locus (14q11) and a region (14q32) of potential importance in leukemogenesis by a 14;14 translocation in a patient with T-cell chronic lymphocytic leukemia and ataxia-telangiectasia

Michael Davey, V. Bertness, K. Nakahara, J. P. Johnson, O. W. McBride, T. A. Waldmann, I. R. Kirsch

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Abstract

We describe a t(14;14)(q11;q32) translocation in a patient with T-cell chronic lymphocytic leukemia and ataxia-telangiectasia (AT). By using a battery of joining (J)-segment probes from the T-cell receptor (TCR) α-chain locus TCRA, three distinct J(α) rearrangements were observed. One rearrangement reflected a normal TCRA variable (V) region V(α)-to-J(α) recombination. The second rearrangement was caused by the translocation event itself, which joined a DNA segment from 14q32 centromeric to the immunoglobulin heavy chain locus (IGH) and a J(α) gene located ≃ 75 kilobases (kb) 5' of the TCRA constant region gene (C(α)). A third rearrangement involved a 17-kb internal deletion 3' to the translocation, a rearrangement within the J(α) locus that has been observed once before in a patient with AT. Analysis of these three rearrangements underscores the increase in aberrant locus-specific recombination in lymphocytes from patients with AT. Furthermore, these studies support the view that a growth-effecting gene is present in the 14q32 region that participates in the leukemogenic process.

Original languageEnglish (US)
Pages (from-to)9287-9291
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume85
Issue number23
StatePublished - 1988
Externally publishedYes

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T-Cell Prolymphocytic Leukemia
Ataxia Telangiectasia
T-Cell Antigen Receptor
Genetic Recombination
Genes
Immunoglobulin Heavy Chains
Lymphocytes
DNA
Growth

ASJC Scopus subject areas

  • General
  • Genetics

Cite this

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title = "Juxtaposition of the T-cell receptor α-chain locus (14q11) and a region (14q32) of potential importance in leukemogenesis by a 14;14 translocation in a patient with T-cell chronic lymphocytic leukemia and ataxia-telangiectasia",
abstract = "We describe a t(14;14)(q11;q32) translocation in a patient with T-cell chronic lymphocytic leukemia and ataxia-telangiectasia (AT). By using a battery of joining (J)-segment probes from the T-cell receptor (TCR) α-chain locus TCRA, three distinct J(α) rearrangements were observed. One rearrangement reflected a normal TCRA variable (V) region V(α)-to-J(α) recombination. The second rearrangement was caused by the translocation event itself, which joined a DNA segment from 14q32 centromeric to the immunoglobulin heavy chain locus (IGH) and a J(α) gene located ≃ 75 kilobases (kb) 5' of the TCRA constant region gene (C(α)). A third rearrangement involved a 17-kb internal deletion 3' to the translocation, a rearrangement within the J(α) locus that has been observed once before in a patient with AT. Analysis of these three rearrangements underscores the increase in aberrant locus-specific recombination in lymphocytes from patients with AT. Furthermore, these studies support the view that a growth-effecting gene is present in the 14q32 region that participates in the leukemogenic process.",
author = "Michael Davey and V. Bertness and K. Nakahara and Johnson, {J. P.} and McBride, {O. W.} and Waldmann, {T. A.} and Kirsch, {I. R.}",
year = "1988",
language = "English (US)",
volume = "85",
pages = "9287--9291",
journal = "Proceedings of the National Academy of Sciences of the United States of America",
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T1 - Juxtaposition of the T-cell receptor α-chain locus (14q11) and a region (14q32) of potential importance in leukemogenesis by a 14;14 translocation in a patient with T-cell chronic lymphocytic leukemia and ataxia-telangiectasia

AU - Davey, Michael

AU - Bertness, V.

AU - Nakahara, K.

AU - Johnson, J. P.

AU - McBride, O. W.

AU - Waldmann, T. A.

AU - Kirsch, I. R.

PY - 1988

Y1 - 1988

N2 - We describe a t(14;14)(q11;q32) translocation in a patient with T-cell chronic lymphocytic leukemia and ataxia-telangiectasia (AT). By using a battery of joining (J)-segment probes from the T-cell receptor (TCR) α-chain locus TCRA, three distinct J(α) rearrangements were observed. One rearrangement reflected a normal TCRA variable (V) region V(α)-to-J(α) recombination. The second rearrangement was caused by the translocation event itself, which joined a DNA segment from 14q32 centromeric to the immunoglobulin heavy chain locus (IGH) and a J(α) gene located ≃ 75 kilobases (kb) 5' of the TCRA constant region gene (C(α)). A third rearrangement involved a 17-kb internal deletion 3' to the translocation, a rearrangement within the J(α) locus that has been observed once before in a patient with AT. Analysis of these three rearrangements underscores the increase in aberrant locus-specific recombination in lymphocytes from patients with AT. Furthermore, these studies support the view that a growth-effecting gene is present in the 14q32 region that participates in the leukemogenic process.

AB - We describe a t(14;14)(q11;q32) translocation in a patient with T-cell chronic lymphocytic leukemia and ataxia-telangiectasia (AT). By using a battery of joining (J)-segment probes from the T-cell receptor (TCR) α-chain locus TCRA, three distinct J(α) rearrangements were observed. One rearrangement reflected a normal TCRA variable (V) region V(α)-to-J(α) recombination. The second rearrangement was caused by the translocation event itself, which joined a DNA segment from 14q32 centromeric to the immunoglobulin heavy chain locus (IGH) and a J(α) gene located ≃ 75 kilobases (kb) 5' of the TCRA constant region gene (C(α)). A third rearrangement involved a 17-kb internal deletion 3' to the translocation, a rearrangement within the J(α) locus that has been observed once before in a patient with AT. Analysis of these three rearrangements underscores the increase in aberrant locus-specific recombination in lymphocytes from patients with AT. Furthermore, these studies support the view that a growth-effecting gene is present in the 14q32 region that participates in the leukemogenic process.

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