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Mathas, S. et al.

Mathas, Janz, Hummel, Hummel, Wollert-Wulf, Lusatis, Anagnostopoulos, Lietz, Sigvardsson, Jundt, Jöhrens, Bommert, Stein, Dörken,

Intrinsic inhibition of transcription factor E2A by HLH proteins ABF-1 and Id2 mediates reprogramming of neoplastic B cells in Hodgkin lymphoma.

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.[1]

References

Intrinsic inhibition of transcription factor E2A by HLH proteins ABF-1 and Id2 mediates reprogramming of neoplastic B cells in Hodgkin lymphoma. Mathas, S., Janz, M., Hummel, F., Hummel, M., Wollert-Wulf, B., Lusatis, S., Anagnostopoulos, I., Lietz, A., Sigvardsson, M., Jundt, F., Jöhrens, K., Bommert, K., Stein, H., Dörken, B. Nat. Immunol. (2006) [Pubmed]

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