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Updated: Apr 20, 2026

An Efficient and Simple Method to Establish NK and T Cell Lines from Patients with Chronic Active Epstein-Barr Virus Infection
Published on: March 30, 2018
Epstein-Barr virus and Burkitt lymphoma
Martin Rowe1, Leah Fitzsimmons, Andrew I Bell
1School of Cancer Sciences, University of Bir-mingham CMDS, Vincent Drive, Edgbaston, Birmingham, B15 2TT, UK. m.rowe@bham.ac.uk.
Epstein-Barr virus (EBV) and c-MYC oncogene activation are key factors in Burkitt lymphoma (BL) pathogenesis. Understanding their complex interplay offers new therapeutic strategies for this viral-associated cancer.
Area of Science:
- Oncology
- Virology
- Genetics
Background:
- Epstein-Barr virus (EBV), a human herpesvirus, was discovered in Burkitt lymphoma (BL) cells in 1964.
- BL is characterized by chromosomal translocations leading to c-MYC oncogene activation.
- The discovery of EBV spurred research into viral causes of human cancers.
Purpose of the Study:
- To review the current understanding of EBV's role in BL pathogenesis.
- To examine the involvement of the c-MYC oncogene in BL development.
- To discuss implications for novel therapeutic strategies against BL.
Main Methods:
- Literature review of EBV and c-MYC in Burkitt lymphoma.
- Analysis of oncogenic mechanisms in viral-associated cancers.
- Synthesis of current research on BL pathogenesis.
Main Results:
- EBV is a potent growth-transforming agent for B cells.
- BL pathogenesis involves complex interactions between EBV and cellular oncogenes like c-MYC.
- Characteristic chromosomal translocations in BL result in constitutive c-MYC activation.
Conclusions:
- The pathogenesis of BL is intricate, involving both EBV and c-MYC.
- Understanding these factors is crucial for developing targeted therapies.
- New therapeutic strategies may emerge from dissecting the viral and cellular contributions to BL.
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