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Intrinsic inhibition of transcription factor E2A by HLH proteins ABF-1 and Id2 mediates reprogramming of neoplastic B cells in Hodgkin lymphoma
Max-Delbrück-Center for Molecular Medicine, Berlin.
Max-Delbrück-Center for Molecular Medicine, Berlin.
Medical University Berlin.
Medical University Berlin.
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2006 (English)In: Nature Immunology, ISSN 1529-2908, E-ISSN 1529-2916, Vol. 7, no 2, 207-215 p.Article in journal (Refereed) Published
Abstract [en]

B cell differentiation is controlled by a complex network of lineage-restricted transcription factors. How perturbations to this network alter B cell fate remains poorly understood. Here we show that classical Hodgkin lymphoma tumor cells, which originate from mature B cells, have lost the B cell phenotype as a result of aberrant expression of transcriptional regulators. The B cell-specific transcription factor program was disrupted by overexpression of the helix-loop-helix proteins ABF-1 and Id2. Both factors antagonized the function of the B cell-determining transcription factor E2A. As a result, expression of genes specific to B cells was lost and expression of genes not normally associated with the B lineage was upregulated. These data demonstrate the plasticity of mature human lymphoid cells and offer an explanation for the unique classical Hodgkin lymphoma phenotype.

Place, publisher, year, edition, pages
Nature Publishing Group , 2006. Vol. 7, no 2, 207-215 p.
National Category
Engineering and Technology
Identifiers
URN: urn:nbn:se:liu:diva-74449DOI: 10.1038/ni1285ISI: 000234801700022OAI: oai:DiVA.org:liu-74449DiVA: diva2:484814
Available from: 2012-01-27 Created: 2012-01-27 Last updated: 2017-12-08

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Sigvardsson, Mikael

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