Allie Kreitman ’21; Mahala Moran ’22
Majors: Molecular Biology
Faculty Collaborator: Olivia Hatton, Molecular Biology
EBV was the first oncogenic virus discovered in humans. While EBV remains latent in 90% of the global adult population, it is also associated with several potentially fatal cancers including diffuse large B cell lymphoma (DLBCL), post-transplant lymphoproliferative disorder (PTLD), nasal T/ natural killer (NK) cell lymphoma, and nasopharyngeal carcinoma. Having a thorough understanding of how EBV promotes the characteristic hallmarks of cancer, cellular abilities acquired during tumorigenesis, is necessary for the discovery of rational targeted therapies. In 2011, Hanahan and Weinberg defined 8 hallmarks of cancer – sustaining proliferative signaling, repressing growth suppressors, preventing cell death, enabling replicative immortality, promoting angiogenesis, triggering invasion and metastasis, deregulating cellular energetics, and evading the host immune system – and 2 enabling characteristics – inducing genomic instability and tumor promoting inflammation. Here, we review some mechanisms by which EBV promotes four of these hallmarks in EBV+ B cell lymphomas such as DLBCL and PTLD: evading host immunity, deregulating cellular energetics, resisting cell death, and inducing angiogenesis. Understanding the ways EBV promotes these hallmarks of cancer could provide novel targets for viral-specific therapies in cancer treatment.
