New IGH@ partners in B-cell precursor acute lymphoblastic leukaemia
New IGH@ partners in B-cell precursor acute lymphoblastic leukaemia
Novel and recurrent translocations affecting multiple chromosomes were highlighted with refined FISH mapping identifying putative IGH@ partner genes at, or flanking, the translocation breakpoints. Cytogenetics, metaphase and interphase FISH, using a dual colour break-apart probe specific for IGH@, identified seventeen translocations, seven of which were recurrent. Sequential FISH mapping of four translocations, t(14;19)(q32;q13), t(8;14)(q11;q32), previously reported, and novel translocations, t(14;14)(q11;q32)/inv(14)(q11q32) and t(14;20)(q32;q13) identified the involvement of five members of the same gene family, CAATT enhancer binding protein (CEBP).
Long distance inverse PCR (LDI-PCR) with primers specific for the IGHJ6 gene segment allowed molecular cloning and further evidence to confirm the involvement of genes CEBPA (19q13, n=11), CEBPG (n=1), CEBPD (uq11, n=10), CEBPE (14q11, n=4) and CEBPB (20q13, n=4). Over-expression of the respective target genes was shown by qRT-PCR in those with available material.
The same techniques were applied to the translocation, t(6;14)(p22;q32), previously reported in a single case of B-cell ALL, confirming the recurrent nature of this translocation and the partner gene as inhibitor of DNA binding 4 (Id4). Similarly, CRLF2 was implicated in both translocations, t(X;14)(p22;q32) and t(Y;14)(p11;q32). Another four partner genes to the IGH@ locus were identified: TCRγ(7p14), MILLT10 (10p14), BRCC2 (11q24) and IGF2BP1 (17q21).
This study has led to the identification of multiple partners of the IGH@ locus in BCP-ALL patients, which were previously unknown. Understanding the function of these genes in the lymphoid cell lineage may define a new subgroup of BCP-ALL in which specific drug development may improve outcome.
University of Southampton
2007
Russell, Lisa Jane
(2007)
New IGH@ partners in B-cell precursor acute lymphoblastic leukaemia.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
Novel and recurrent translocations affecting multiple chromosomes were highlighted with refined FISH mapping identifying putative IGH@ partner genes at, or flanking, the translocation breakpoints. Cytogenetics, metaphase and interphase FISH, using a dual colour break-apart probe specific for IGH@, identified seventeen translocations, seven of which were recurrent. Sequential FISH mapping of four translocations, t(14;19)(q32;q13), t(8;14)(q11;q32), previously reported, and novel translocations, t(14;14)(q11;q32)/inv(14)(q11q32) and t(14;20)(q32;q13) identified the involvement of five members of the same gene family, CAATT enhancer binding protein (CEBP).
Long distance inverse PCR (LDI-PCR) with primers specific for the IGHJ6 gene segment allowed molecular cloning and further evidence to confirm the involvement of genes CEBPA (19q13, n=11), CEBPG (n=1), CEBPD (uq11, n=10), CEBPE (14q11, n=4) and CEBPB (20q13, n=4). Over-expression of the respective target genes was shown by qRT-PCR in those with available material.
The same techniques were applied to the translocation, t(6;14)(p22;q32), previously reported in a single case of B-cell ALL, confirming the recurrent nature of this translocation and the partner gene as inhibitor of DNA binding 4 (Id4). Similarly, CRLF2 was implicated in both translocations, t(X;14)(p22;q32) and t(Y;14)(p11;q32). Another four partner genes to the IGH@ locus were identified: TCRγ(7p14), MILLT10 (10p14), BRCC2 (11q24) and IGF2BP1 (17q21).
This study has led to the identification of multiple partners of the IGH@ locus in BCP-ALL patients, which were previously unknown. Understanding the function of these genes in the lymphoid cell lineage may define a new subgroup of BCP-ALL in which specific drug development may improve outcome.
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Published date: 2007
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Local EPrints ID: 466274
URI: http://eprints.soton.ac.uk/id/eprint/466274
PURE UUID: a841ea41-c5fe-4773-a9ad-be44078dc7c3
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Date deposited: 05 Jul 2022 05:01
Last modified: 05 Jul 2022 05:01
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Author:
Lisa Jane Russell
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