The browser you are using is not supported by this website. All versions of Internet Explorer are no longer supported, either by us or Microsoft (read more here: https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Please use a modern browser to fully experience our website, such as the newest versions of Edge, Chrome, Firefox or Safari etc.

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

På svenska

Author

  • Andreas Lietz
  • Martin Janz
  • Mikael Sigvardsson
  • Franziska Jundt
  • Bernd Doerken
  • Stephan Mathas

Summary, in English

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.

Department/s

Publishing year

2007

Language

English

Pages

342-348

Publication/Series

British Journal of Haematology

Volume

137

Issue

4

Document type

Journal article

Publisher

Wiley-Blackwell

Topic

  • Hematology

Keywords

  • E2A
  • lymphoma
  • primary effusion lymphoma
  • Hodgkin lymphoma

Status

Published

ISBN/ISSN/Other

  • ISSN: 0007-1048