Loss of bHLH transcription factor E2A activity in primary effusion lymphoma confers resistance to apoptosis
Författare
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.
Avdelning/ar
Publiceringsår
2007
Språk
Engelska
Sidor
342-348
Publikation/Tidskrift/Serie
British Journal of Haematology
Volym
137
Issue
4
Länkar
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