@article{10902/36487,
year = {2024},
url = {https://hdl.handle.net/10902/36487},
abstract = {The Epstein-Barr virus (EBV) infection does not induce any apparent pathology in most people but it has been associated with an increased risk of developing a number of non-malignant diseases (e.g., infectious mononucleosis and multiple sclerosis) and some cancers. Among these, the association between EBV and Burkitt lymphoma (BL) is striking, involving a tumor where MYC is deregulated by translocation in all cases. BL is more prevalent in children from equatorial Africa (>90% of the cases) whereas the association of EBV with BL is much lower (25-40%) in other regions. This high association suggests that EBV is a driving mechanism, but whether it is sufficient to trigger lymphomagenesis or it is a cooperative factor is under debate. Indeed, the precise molecular mechanisms underlying the virus activity in infected B cells in collaboration with MYC is still unclear. The molecular mechanisms by which EBV operates in tumor B cells will be discussed.},
organization = {Funding: This research was funded by MICIU/AEI/10.13039/501100011033, grant number PID2020- 115903GB-100 to J.L. Acknowledgments: BioRender was used for the generation of most figures included in this manuscript (created in BioRender. Garcia, L. (2024) BioRender.com/y04j261)},
publisher = {MDPI},
publisher = {Cancers, 2024, 16(24), 4212},
title = {The functional interaction between Epstein–Barr virus and MYC in the pathogenesis of Burkitt lymphoma},
author = {Solares, Sandra and León Serrano, Javier and García Gutierrez, Lucía},
}