The functional interaction between Epstein–Barr virus and MYC in the pathogenesis of Burkitt lymphoma
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 betwe...
| Autores: | , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2024 |
| País: | España |
| Institución: | Universidad de Cantabria (UC) |
| Repositorio: | UCrea Repositorio Abierto de la Universidad de Cantabria |
| Idioma: | inglés |
| OAI Identifier: | oai:repositorio.unican.es:10902/36487 |
| Acceso en línea: | https://hdl.handle.net/10902/36487 |
| Access Level: | acceso abierto |
| Palabra clave: | MYC Epstein–Barr virus Burkitt lymphoma |
| Sumario: | 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. |
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