c-MYC is believed to be responsible for the lymphoma because : c-MYC dysregulation which induces lymphomagenesis by loss of the tight control.
Burkitt lymphoma is a germinal center B-cell-derived cancer that was instrumental in the identification of MYC as an important human oncogene more than three decades ago.
Recently, new genomics technologies have uncovered several additional oncogenic mechanisms that cooperate with MYC to create this highly aggressive cancer. The transcription factor TCF-3 is central to Burkitt lymphoma pathogenesis.
TCF-3 is rendered constitutively active in Burkitt lymphoma by two related mechanisms: somatic mutations that inactivate its negative regulator ID3, and somatic mutations in TCF-3 that block the ability of ID3 to bind and interfere with its activity as a transcription factor.
TCF-3 is also a master regulator of normal germinal center B-cell differentiation. Within the germinal center, TCF-3 up-regulates genes that are characteristically expressed in the rapidly dividing centroblasts, the putative cell of origin for Burkitt lymphoma, while repressing genes expressed in the less proliferative centrocytes.
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