期刊
SEMINARS IN CANCER BIOLOGY
卷 19, 期 6, 页码 389-393出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.semcancer.2009.07.006
关键词
Burkitt's lymphoma; Epstein-Barr virus; Tumor virus; Tumor survival
类别
资金
- National Cancer Institute, National Institutes of Health [P01 CA022443, R01 CA133027, R01 CA070723]
- National Cancer Center
- NATIONAL CANCER INSTITUTE [R01CA070723, R01CA133027, P01CA022443] Funding Source: NIH RePORTER
We have found that not all Epstein-Barr viral (EBV) plasmids are duplicated each cell cycle. This inefficiency is intrinsic to EBV's mechanism of DNA synthesis in latently infected cells and necessarily leads to a loss of EBV plasmids from proliferating cells. If EBV provides its host cells advantages that allow those cells that retain EBV to outgrow those that lose it, then such proliferating populations will be EBV-positive. EBV-associated human tumors are EBV-positive. Thus, the presence of EBV plasmids in most cells of a tumor demonstrates that EBV sustains these tumors in vivo. The virus can provide multiple selective advantages to tumor cells, including promoting cell proliferation and inhibiting cell death. In the case of Burkitt's lymphomas (BL), most current evidence indicates that the tumor requires the virus minimally to block apoptosis. (C) 2009 Elsevier Ltd. All rights reserved.
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