(ChemotherapyAdvisor) – The survival mechanisms of Burkitt lymphoma have been elucidated, according to an international team of researchers. This conclusion is based on a study entitled “Synergy between PI3K Signaling and MYC in Burkitt Lymphomagenesis,” which was published online in Cancer Cell on August 14.

Burkitt lymphoma is a fast-growing, malignant B-cell-derived tumor formed in the germinal centers of several lymphatic tissues throughout the body. In normal B-cells, expression of a gene known as c-MYC leads to programmed cell death (apoptosis). However, when there are breaks in B-cell DNA, c-MYC is translocated to a new position in the genome. At this new position, overexpression of c-MYC leads to massive cell death. To play an oncogenic role, the proapoptotic activity of translocated c-MYC must be counterbalanced by survival signals.

In this study, the investigators aimed to determine the nature of these survival signals in Burkitt lymphoma-like tumors. The investigators hypothesized that survival signals in these tumors might be delivered by a protein known as PI3K, which causes mature B cells to overcome proapoptotic signals from c-MYC.

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The investigators found that their hypothesis was indeed correct. In mouse germinal center B-cells, they observed that combining overexpressed c-MYC and PI3K activity led to the development of Burkitt lymphoma-like tumors. According to the investigators, these tumors are similar to human Burkitt lymphoma in histology, surface and other markers, and gene expression profile.

“These results and our finding of recurrent PI3K pathway activation in human BL indicate that deregulated c-MYC and PI3K activity cooperate in Burkitt lymphoma pathogenesis,” the investigators concluded.