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Loss of bHLH transcription factor E2A activity in primary effusion lymphoma confers resistance to apoptosis
Lund University.
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2007 (English)In: British Journal of Haematology, ISSN 0007-1048, E-ISSN 1365-2141, Vol. 137, no 4, 342-348 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2007. Vol. 137, no 4, 342-348 p.
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Medical and Health Sciences
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URN: urn:nbn:se:liu:diva-39977DOI: 10.1111/j.1365-2141.2007.06583.xLocal ID: 51896OAI: oai:DiVA.org:liu-39977DiVA: diva2:260826
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13

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Sigvardsson, Mikael

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