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Fifth International Symposium on Childhood, Adolescent and Young Adult Non-Hodgkin Lymphoma Abstracts, 22 October 2015, Varese, Italy.

Burkitt lymphoma (BL) is an aggressive B cell lymphoma of germinal center (GC) origin which occurs at high incidence in Equatorial Africa and low incidence elsewhere. It has been characterized in detail, and defined by its gene expression pattern. BL occurs at all ages, from 2 years to approximately 70 years (few Africans lived longer) its peak age is 7 years of age and it accounts for 50% of childhood cancers and 80% of childhood lymphomas in equatorial African regions, especially where climatic conditions are favorable to insect vectors of a number of tropical diseases, including malaria. Malaria has for long been associated with BL although evidence is indirect (e.g., higher incidence of BL in high intensity malarial region). Elsewhere in the world, although the incidence is much lower, BL is the most frequent childhood NHL, based on the relatively limited data available. In 1964, a new herpes virus–Epstein Barr virus, was discovered in BL cell lines derived from Ugandan tumors and shown by serological studies to be ubiquitous although varying markedly in the age of acquisition, which is a function of socioeconomic status. Since most countries are of low socioeconomic status, the majority of cases of BL throughout the world contain EBV DNA in their tumors cells, but EBV+ BL is uncommon in high income countries, except in BL related to HIV infection, in which approximately 30% of tumours are EBV+. EBV survives indefinitely in memory B cells, which it reaches by using a subset of its latent genes to protect virus-transformed na€ıve B cells (which would otherwise undergo mutation) from apoptosis during passage across the GC. Such cells are invisible to the immune system since they express no EBV proteins except EBNA1 which is only expressed during intermittent clonal expansion to maintain equal numbers of EBV+ cells in progeny. MYC appears to be relevant to affinity selection of antibodies, a process which also takes place in GCs, and is normally expressed only in a small fraction of cells in the light zone. Mutations in the hypervariable region are generated by activation dependent cytidine kinase (AID) then cells undergo multiple rounds of cell cycling during which only cells able to bind with high affinity to the antigen survive and progress from the light zone to dark zone where they proliferate. In BL a MYC-Ig translocation in addition to mutations in MYC (which is normally switched off by BCL6 when the cell enters a dark zone) decouple MYC from this pathway and MYC is constitutively activated, maintaining cell division. This is not sufficient to lead to true neoplasia, which requires activation of PI3K, in part driven by tonic activation of the B cell receptor. Activating mutations of PI3K, which drives proliferation via the AKT/mTOR pathway, as well as in TCF-3 and in turn cyclin D3, which ensures traversal of the G1-S checkpoint are all key elements of BL pathogenesis. Finally, exposure of GC cells along with CD40 and IL4 (equivalent to T cell help) to malaria extracts including haemozoin derived from hemoglobin, drive B cell proliferation, stimulate cytokine and AID production and increase the risk of MYC-IG translocations. Both EBV and malaria increase the number of circulating EBV containing cells. These findings correlate well with epidemiological observations.