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Molecular cytogenetic characterization of TCF3 (E2A)/19p13.3 rearrangements in B-cell precursor acute lymphoblastic leukemia

Molecular cytogenetic characterization of TCF3 (E2A)/19p13.3 rearrangements in B-cell precursor acute lymphoblastic leukemia
Molecular cytogenetic characterization of TCF3 (E2A)/19p13.3 rearrangements in B-cell precursor acute lymphoblastic leukemia
The t(1; 19)(q23;p 13.3) is one of the most common chromosomal abnormalities in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and usually gives rise to the TCF3-PBXI fusion gene. Additional rare, and sometimes cytogenetically cryptic, translocations involving the TCF3 gene have also been described. Using a dual color split-signal fluorescence in situ hybridization (FISH) probe, we have investigated the involvement of this gene in a series of BCP-ALLs harboring 19p 13 translocations, as well as an unselected patient cohort. The TCF3 gene was shown to be involved in the majority of cases with a cytogenetically visible t(1; 19) translocation, while the remaining TCF3-negative ALLs demonstrated breakpoint heterogeneity. Although most "other" 19p 13 translocations did not produce a split-signal FISH pattern, a novel t(13; 1 9)(q 14;p 13) involving TCF3 was discovered. A prospective screen of 161 children with BCP-ALL revealed a cryptic t(12; 19)(p13;p 13), another novel TCF3 rearrangement, and a series of patients with submicroscopic deletions of TCF3. These results demonstrate the utility of a split-signal FISH strategy in confirming the involvement of the TCF3 gene in 19p 13 rearrangements and in identifying novel and cryptic TCF3 translocations. In addition to its role as a fusion partner gene, we propose that TCF3 can also act as a tumor suppressor gene in BCP-ALL. (c) 2007 Wiley-Liss, Inc
acute lymphoblastic leukemia, pre-b, fusion gene, identification, polymerase chain-reaction, translocation, tumor-suppressor, leukemia, chromosomal-abnormalities, 19)(q23, e2a gene, t(1, hybridization, prognostic-significance, p13.3), children, molecular cytogenetic characterization, patient, fusion, fish, deletions, time, b cell, gene, abnormalities
1045-2257
478-486
Barber, Kerry E.
68bc6851-3dd1-4767-ad97-8de1918224db
Harrison, Christine J.
52da7673-509c-4b88-b92e-0c021c9c7d3e
Broadfield, Zoe J.
27b59649-1631-4036-a599-f5f81c1b9992
Stewart, Adam R.M.
201f6d8b-8004-4605-bfff-dd82c711bade
Wright, Sarah L.
56f2b242-4d7d-46be-838b-9064ff96d152
Martineau, Mary
6cc6f57f-7b57-4583-81eb-17dac737e35c
Strefford, Jon C.
3782b392-f080-42bf-bdca-8aa5d6ca532f
Moorman, Anthony V.
e4ced178-ee03-47ef-bc5e-25d8453951d5
Barber, Kerry E.
68bc6851-3dd1-4767-ad97-8de1918224db
Harrison, Christine J.
52da7673-509c-4b88-b92e-0c021c9c7d3e
Broadfield, Zoe J.
27b59649-1631-4036-a599-f5f81c1b9992
Stewart, Adam R.M.
201f6d8b-8004-4605-bfff-dd82c711bade
Wright, Sarah L.
56f2b242-4d7d-46be-838b-9064ff96d152
Martineau, Mary
6cc6f57f-7b57-4583-81eb-17dac737e35c
Strefford, Jon C.
3782b392-f080-42bf-bdca-8aa5d6ca532f
Moorman, Anthony V.
e4ced178-ee03-47ef-bc5e-25d8453951d5

Barber, Kerry E., Harrison, Christine J., Broadfield, Zoe J., Stewart, Adam R.M., Wright, Sarah L., Martineau, Mary, Strefford, Jon C. and Moorman, Anthony V. (2007) Molecular cytogenetic characterization of TCF3 (E2A)/19p13.3 rearrangements in B-cell precursor acute lymphoblastic leukemia. Genes, Chromosomes and Cancer, 46 (5), 478-486. (doi:10.1002/gcc.20431).

Record type: Article

Abstract

The t(1; 19)(q23;p 13.3) is one of the most common chromosomal abnormalities in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) and usually gives rise to the TCF3-PBXI fusion gene. Additional rare, and sometimes cytogenetically cryptic, translocations involving the TCF3 gene have also been described. Using a dual color split-signal fluorescence in situ hybridization (FISH) probe, we have investigated the involvement of this gene in a series of BCP-ALLs harboring 19p 13 translocations, as well as an unselected patient cohort. The TCF3 gene was shown to be involved in the majority of cases with a cytogenetically visible t(1; 19) translocation, while the remaining TCF3-negative ALLs demonstrated breakpoint heterogeneity. Although most "other" 19p 13 translocations did not produce a split-signal FISH pattern, a novel t(13; 1 9)(q 14;p 13) involving TCF3 was discovered. A prospective screen of 161 children with BCP-ALL revealed a cryptic t(12; 19)(p13;p 13), another novel TCF3 rearrangement, and a series of patients with submicroscopic deletions of TCF3. These results demonstrate the utility of a split-signal FISH strategy in confirming the involvement of the TCF3 gene in 19p 13 rearrangements and in identifying novel and cryptic TCF3 translocations. In addition to its role as a fusion partner gene, we propose that TCF3 can also act as a tumor suppressor gene in BCP-ALL. (c) 2007 Wiley-Liss, Inc

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More information

Published date: 20 February 2007
Keywords: acute lymphoblastic leukemia, pre-b, fusion gene, identification, polymerase chain-reaction, translocation, tumor-suppressor, leukemia, chromosomal-abnormalities, 19)(q23, e2a gene, t(1, hybridization, prognostic-significance, p13.3), children, molecular cytogenetic characterization, patient, fusion, fish, deletions, time, b cell, gene, abnormalities

Identifiers

Local EPrints ID: 62682
URI: https://eprints.soton.ac.uk/id/eprint/62682
ISSN: 1045-2257
PURE UUID: 86610532-6906-4c24-ab2c-a50cec575c97
ORCID for Jon C. Strefford: ORCID iD orcid.org/0000-0002-0972-2881

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Date deposited: 05 Sep 2008
Last modified: 14 Mar 2019 01:43

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Contributors

Author: Kerry E. Barber
Author: Christine J. Harrison
Author: Zoe J. Broadfield
Author: Adam R.M. Stewart
Author: Sarah L. Wright
Author: Mary Martineau
Author: Anthony V. Moorman

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