Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010:108:1-19.
doi: 10.1016/B978-0-12-380888-2.00001-7.

Insights into the evolution of lymphomas induced by Epstein-Barr virus

David Vereide  1 , Bill Sugden
Affiliations
Review

Insights into the evolution of lymphomas induced by Epstein-Barr virus

David Vereide et al. Adv Cancer Res. 2010.

Abstract

Epstein-Barr virus (EBV) encodes a wealth of oncogenic instructions, including the abilities to drive a resting normal B cell to proliferate and to override apoptotic stimuli. EBV is found in almost all types of lymphomas at varying frequencies. However, the particular viral genes expressed differ considerably among tumors. We have examined the role of EBV in several lymphomas by conditionally evicting the extrachromosomal viral genome from tumor cells in vitro and have found a graded dependence on the virus. Tumor cells that express all the known latent viral genes have been found to depend on the virus to drive proliferation and to block apoptosis at least in part by repressing the proapoptotic protein Bim. Other tumor cells, which express fewer viral genes, also depend on the virus to block apoptosis, but rely on the virus to promote but not to drive proliferation. Lastly, tumor cells with the fewest viral genes expressed have been found to require EBV to prevent the inefficient induction of a Bim-independent apoptosis. We present a model for the evolution of EBV-induced lymphomas in which tumors are initially "addicted" to the virus for almost all oncogenic functions. These tumors are targets for the immune system because they express multiple immunogenic viral proteins. Therefore, EBV-induced tumors are under selective pressure to acquire cellular mutations that can replace viral functions. We posit that the heterogeneity in viral gene expression among different EBV-associated lymphomas reflects a dynamic process by which tumors evolve to be less dependent on the virus.

PubMed Disclaimer

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

Publication types