The cellular myelocytomatosis (c-myc) oncogene plays a vital role in cellular proliferation, differentiation, apoptosis and acts as transcriptional regulator of gene expression. c-Myc expression is essential and sufficient to assist most of the cells to enter synthetic (S) phase of the cell cycle. The encoded protein plays a crucial role in vasculogenesis and angiogenesis during cancer development and progression. c-Myc interacts with its binding partner Max and activates the transcription of growth promoting genes such as cyclin D2, ornithine decarboxylase and E2F1 and it also represses the transcription of multiple genes, especially p21 and p27, by binding to the transcription initiator element (Inr) in a complex with Max and either Sp1 or Miz1. Overexpression of MYC in DLBCL (diffuse large B-cell lymphoma) results in poor outcome and invasive treatment when medicated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP).
