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Perspectives
Reprogramming of B Lymphoid Cells in Human Lymphoma Pathogenesis
Martin Janz, Bernd Dörken and Stephan Mathas
volume 5 | issue 10
15 may 2006Pages: 1057 - 1061
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Previous hypotheses have stated that differentiated cells lose the ability to change their fate. Using lymphoid development as a model system, recent data have challenged this rigid view of cellular differentiation. It has been shown in mouse models that, under certain conditions, even mature lymphoid cells can display a broad developmental potential, and might even transdifferentiate into other cell types. The relevance of these observations for the physiological ontogenesis of lymhpoid cells or their malignant transformation is currently unclear. Recent data from our laboratory have demonstrated that similar processes can be observed in the malignant Hodgkin/Reed-Sternberg cells of classical Hodgkin lymphoma (cHL), a common B cell-derived lymphoma. In HRS cells, the B cell-specific homodimer activity of the transcription factor E2A is functionally disrupted by overexpression of the E2A antagonists activated B cell factor 1 (ABF-1) and inhibitor of differentiation 2 (Id2). In consequence, the expression of B cell-specific genes is lost, and B lineage-inappropriate genes are upregulated. These data have demonstrated the plasiticity of human lymphoid cells and offer an explanation for the unique phenotype of cHL. We first summarize data showing the plasticity of lymphoid cells in mouse models, second describe our observations regarding the altered B cell-specific transcription factor network in HRS cells, and third discuss the possible implications of these findings for human lymphoma pathogenesis.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.