Researchers at the University of Pennsylvania School of Medicine have identified a link between a critical cancer pathway and an Epstein-Barr Virus (EBV) protein known to be expressed in a number of EBV-associated cancers.
Their findings demonstrate a new mechanism by which EBV transforms human B cells from the immune system into cancerous cells, which can lead to development of B-cell lymphomas.
Erle S. Robertson, PhD, Associate Professor of Microbiology and Director of Tumor Virology, with Penn's Abramson Cancer Center and MD/PhD student Jason Knight, published their results in the early March issue of Molecular and Cellular Biology.
Using human cell cultures infected with the Epstein-Barr virus, the investigators found that a specific viral protein targets a molecule that normally regulates the cell-cycle progression, or duplication process, of resting B cells. In the presence of this viral protein – called EBNA3C (for EBV nuclear antigen) – the cell cycle of the usually quiescent human B cells gets a jump start, which ultimately initiates uncontrolled growth.
EBV, a member of the herpesvirus family and one of the most common human viruses, plays a role in cancers such as lymphoproliferative diseases in transplant or AIDS patients, Burkitt's lymphoma, Hodgkin's lymphoma, and nasopharyngeal carcinoma, and also causes the well-known disease, infectious mononucleosis. As many as 95 percent of adults 20 years and older have been infected with EBV, but show no symptoms.