MYC was found to be involved in many germinal center derived lymphomas, and more recently in the histological transformation of indolent mature B-cell malignancies, such as follicular lymphoma (FL), chronic lymphocytic leukemia (CLL) and mucosa-associated lymphoid tissue lymphoma (MALT) to aggressive diffuse large B-cell lymphoma (DLBCL). Pathological MYC activity gain in lymphomas is able to overcome its regulation by repressors, which leads to bypassing the affinity-based selection of B-cells. Arguably the MYC activity gain is the most constantly observed phenomenon (>70% of cases) in transformed FL/MALT/CLL (Richter's transformation) and co-occurs with specific aberrations such as the loss of p53, CDKN2A/B, or gain of BCL2/BCL6. Here we summarize recent progress in the understanding of MYC regulatory network in lymphoma B-cells and highlight its involvement in lymphomas' histological transformation by regulating cyclins, CDKs, p21, p27, BCL2, E2F, FOXP1, BCR signaling components, and non-coding microRNA (miRNA) genes such as miR-150, miR-29, miR-17-92, and miR-34a.

• MeSH
• B-Lymphocytes MeSH
• Leukemia, Lymphocytic, Chronic, B-Cell * MeSH
• Lymphoma, Large B-Cell, Diffuse * MeSH
• Lymphoma, Follicular * MeSH
• Forkhead Transcription Factors MeSH
• Humans MeSH
• Lymphoma, B-Cell, Marginal Zone * MeSH
• Proto-Oncogene Proteins c-myc * MeSH
• Repressor Proteins MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH