Oncogenesis of Lymphoma

Dear Colleagues,

Advances in the fields of molecular genetics, immunology and virology have clarified the mechanisms involved in lymphomagenesis. Human lymphomas have been found to be heterogeneous, not only pathologically but also in terms of pathogenetic pathways, cellular derivation and the tumor microenvironment. Traditionally, some types of lymphomas, such as follicular lymphomas and mantle cell lymphomas, are consistently correlated with genetic abnormalities involving BCL2 and BCL1, respectively. It is well known that the molecular pathway in Burkitt lymphoma involves activation of MYC, inactivation of p53 and infection by EBV. Furthermore, in diffuse large B-cell lymphomas (DLBCL), molecular studies have shown rearrangements in BCL2, BCL6 and MYC genes. Recent studies with NGS and mutational profiling have identified clinically significant genetic subgroups. Four major genetic subgroups have been demonstrated in DLBCL. They are based on 1) mutations in MYD88 and CD79B, 2) BCL6 fusions and NOTCH2 mutations, 3) NOTCH1 mutations and 4) EZH2 mutations/BCL2 rearrangement. A new concept, viral cooperation, has been revealed in lymphomagenesis by molecular virologic studies on primary effusion lymphomas (PELs). In immune-deficient/dysregulated patients, PEL tumor cells, in addition to consistent infection by KSHV/HHV8, are also commonly infected by EBV. Finally, recent insights from genetics, epigenetics and knowledge in the cellular microenvironment have led to the refinement of diagnostic definition and, hopefully, appropriate therapy.

Dr. Annunziata Gloghini
Prof. Dr. Giancarlo Pruneri
Guest Editors

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• lymphomagenesis
• molecular genetics
• immunology
• molecular virology
• KSHV/HHV8
• EBV
• HIV
• pathogenetic pathways
• genotypic subgroups
• tumor microenvironment
• follicular lymphoma
• mantle cell lymphoma
• diffuse large B-cell lymphoma
• targeted therapy
• drug target