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

Författare

  • 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.

Publiceringsår

2007

Språk

Engelska

Sidor

342-348

Publikation/Tidskrift/Serie

British Journal of Haematology

Volym

137

Issue

4

Dokumenttyp

Artikel i tidskrift

Förlag

Wiley-Blackwell

Ämne

  • Hematology

Nyckelord

  • E2A
  • lymphoma
  • primary effusion lymphoma
  • Hodgkin lymphoma

Status

Published

ISBN/ISSN/Övrigt

  • ISSN: 0007-1048