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Molecular cytogenetic characterization of t(14;19)(q32;p13), a new recurrent translocation in B cell malignancies

Micci, Francesca; Panagopoulos, Ioannis LU ; Tjonnfjord, Geir E.; Kolstad, Arne; Delabie, Jan; Beiske, Klaus and Heim, Sverre (2007) In Virchows Archiv: an international journal of pathology 450(5). p.559-565
Abstract
Translocations involving an immunoglobulin (IG) locus are a recurring theme in B cell neoplasia. The rearrangements lead to the joining of an IG gene with a (proto)oncogene, whereby the latter comes under the influence of transcription-stimulating sequences in the constitutively active IG locus resulting in deregulation of the oncogene and neoplastic growth. We present here three cases of B cell neoplasia that showed a t(14;19)(q32;p13) by karyotypic analysis. Detailed molecular cytogenetic characterization of the breakpoints on chromosomes 14 and 19 in the two cases from which extra material was available, demonstrated the involvement of the immunoglobulin heavy-chain (IGH@)-variable region on chromosome 14 in both and, in one case, that... (More)
Translocations involving an immunoglobulin (IG) locus are a recurring theme in B cell neoplasia. The rearrangements lead to the joining of an IG gene with a (proto)oncogene, whereby the latter comes under the influence of transcription-stimulating sequences in the constitutively active IG locus resulting in deregulation of the oncogene and neoplastic growth. We present here three cases of B cell neoplasia that showed a t(14;19)(q32;p13) by karyotypic analysis. Detailed molecular cytogenetic characterization of the breakpoints on chromosomes 14 and 19 in the two cases from which extra material was available, demonstrated the involvement of the immunoglobulin heavy-chain (IGH@)-variable region on chromosome 14 in both and, in one case, that the breakpoint was within the BRD4 gene on chromosome 19. Against the background of what one knows about IGH@ involvement in lymphatic malignancies, it is difficult to envisage a fusion gene with qualitatively altered protein product as the crucial pathogenetic outcome of the translocation. In spite of the fact that we found BRD4 split by the t(14;19)(q32;p13) in one of the two informative cases, we cannot be sure that this was the pathogenetically relevant target gene. Other pathogenetic possibilities could be deregulation of the neighboring NOTCH3 and/or ABHD9 genes, located distal to BRD4 in 19p13. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
19)(q32, t(14, cytogenetics, ALL, large B cell lymphoma, p13), BRD4
in
Virchows Archiv: an international journal of pathology
volume
450
issue
5
pages
559 - 565
publisher
Springer
external identifiers
  • wos:000246113400008
  • scopus:34247639534
ISSN
1432-2307
DOI
10.1007/s00428-007-0407-6
language
English
LU publication?
yes
id
397dcdda-a631-4af5-9423-af25bb8cac42 (old id 662866)
date added to LUP
2007-12-14 09:04:33
date last changed
2017-04-09 04:16:39
@article{397dcdda-a631-4af5-9423-af25bb8cac42,
  abstract     = {Translocations involving an immunoglobulin (IG) locus are a recurring theme in B cell neoplasia. The rearrangements lead to the joining of an IG gene with a (proto)oncogene, whereby the latter comes under the influence of transcription-stimulating sequences in the constitutively active IG locus resulting in deregulation of the oncogene and neoplastic growth. We present here three cases of B cell neoplasia that showed a t(14;19)(q32;p13) by karyotypic analysis. Detailed molecular cytogenetic characterization of the breakpoints on chromosomes 14 and 19 in the two cases from which extra material was available, demonstrated the involvement of the immunoglobulin heavy-chain (IGH@)-variable region on chromosome 14 in both and, in one case, that the breakpoint was within the BRD4 gene on chromosome 19. Against the background of what one knows about IGH@ involvement in lymphatic malignancies, it is difficult to envisage a fusion gene with qualitatively altered protein product as the crucial pathogenetic outcome of the translocation. In spite of the fact that we found BRD4 split by the t(14;19)(q32;p13) in one of the two informative cases, we cannot be sure that this was the pathogenetically relevant target gene. Other pathogenetic possibilities could be deregulation of the neighboring NOTCH3 and/or ABHD9 genes, located distal to BRD4 in 19p13.},
  author       = {Micci, Francesca and Panagopoulos, Ioannis and Tjonnfjord, Geir E. and Kolstad, Arne and Delabie, Jan and Beiske, Klaus and Heim, Sverre},
  issn         = {1432-2307},
  keyword      = {19)(q32,t(14,cytogenetics,ALL,large B cell lymphoma,p13),BRD4},
  language     = {eng},
  number       = {5},
  pages        = {559--565},
  publisher    = {Springer},
  series       = {Virchows Archiv:  an international journal of pathology},
  title        = {Molecular cytogenetic characterization of t(14;19)(q32;p13), a new recurrent translocation in B cell malignancies},
  url          = {http://dx.doi.org/10.1007/s00428-007-0407-6},
  volume       = {450},
  year         = {2007},
}