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Loss of bHLH transcription factor E2A activity in primary effusion lymphoma confers resistance to apoptosis

Lietz, Andreas; Janz, Martin; Sigvardsson, Mikael LU ; Jundt, Franziska; Doerken, Bernd and Mathas, Stephan (2007) In British Journal of Haematology 137(4). p.342-348
Abstract
Similar to classical Hodgkin lymphoma (HL) tumour cells, primary effusion lymphoma (PEL) originates from mature B cells but displays a non-B cell phenotype, the mechanisms and consequences of which are not yet understood. This study showed that PEL lacked DNA binding activity of the B cell-determining transcription factors E2A, EBF and Pax5. PEL overexpressed the E2A antagonists ABF-1 and Id2, which have been described to block the B-cell differentiation program in classical HL. However, in contrast to HL cells, B lineage-inappropriate genes were not similarly upregulated in PEL, and reconstitution of B cell-specific E2A homodimer activity in PEL induced apoptosis. These data demonstrate that lineage infidelity in PEL is not as pronounced... (More)
Similar to classical Hodgkin lymphoma (HL) tumour cells, primary effusion lymphoma (PEL) originates from mature B cells but displays a non-B cell phenotype, the mechanisms and consequences of which are not yet understood. This study showed that PEL lacked DNA binding activity of the B cell-determining transcription factors E2A, EBF and Pax5. PEL overexpressed the E2A antagonists ABF-1 and Id2, which have been described to block the B-cell differentiation program in classical HL. However, in contrast to HL cells, B lineage-inappropriate genes were not similarly upregulated in PEL, and reconstitution of B cell-specific E2A homodimer activity in PEL induced apoptosis. These data demonstrate that lineage infidelity in PEL is not as pronounced as in HL, and that the loss of the B cell-specific transcription factor E2A in PEL is implicated in apoptosis protection. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
E2A, lymphoma, primary effusion lymphoma, Hodgkin lymphoma
in
British Journal of Haematology
volume
137
issue
4
pages
342 - 348
publisher
Federation of European Neuroscience Societies and Blackwell Publishing Ltd
external identifiers
  • wos:000245938900008
  • scopus:34247474476
ISSN
0007-1048
DOI
10.1111/j.1365-2141.2007.06583.x
language
English
LU publication?
yes
id
771b9f7f-4223-4ec7-aee9-586580bbd1fa (old id 663194)
date added to LUP
2007-12-12 14:39:11
date last changed
2017-01-01 04:53:11
@article{771b9f7f-4223-4ec7-aee9-586580bbd1fa,
  abstract     = {Similar to classical Hodgkin lymphoma (HL) tumour cells, primary effusion lymphoma (PEL) originates from mature B cells but displays a non-B cell phenotype, the mechanisms and consequences of which are not yet understood. This study showed that PEL lacked DNA binding activity of the B cell-determining transcription factors E2A, EBF and Pax5. PEL overexpressed the E2A antagonists ABF-1 and Id2, which have been described to block the B-cell differentiation program in classical HL. However, in contrast to HL cells, B lineage-inappropriate genes were not similarly upregulated in PEL, and reconstitution of B cell-specific E2A homodimer activity in PEL induced apoptosis. These data demonstrate that lineage infidelity in PEL is not as pronounced as in HL, and that the loss of the B cell-specific transcription factor E2A in PEL is implicated in apoptosis protection.},
  author       = {Lietz, Andreas and Janz, Martin and Sigvardsson, Mikael and Jundt, Franziska and Doerken, Bernd and Mathas, Stephan},
  issn         = {0007-1048},
  keyword      = {E2A,lymphoma,primary effusion lymphoma,Hodgkin lymphoma},
  language     = {eng},
  number       = {4},
  pages        = {342--348},
  publisher    = {Federation of European Neuroscience Societies and Blackwell Publishing Ltd},
  series       = {British Journal of Haematology},
  title        = {Loss of bHLH transcription factor E2A activity in primary effusion lymphoma confers resistance to apoptosis},
  url          = {http://dx.doi.org/10.1111/j.1365-2141.2007.06583.x},
  volume       = {137},
  year         = {2007},
}