FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |   Search Term  Advanced Search

Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe

Previous Volume 350:2621 June 17, 2004 Number 25 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

	Full Text PDF PDA Full Text Purchase this article Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited E-mail When Letters Appear Related Article by Thorley-Lawson, D. A. PubMed Citation

To the Editor: In their review of the persistence of the Epstein–Barr virus (EBV) and the origins of associated lymphomas (March 25 issue),¹ Thorley-Lawson and Gross state, "There is no satisfactory explanation of how EBV participates in the pathogenesis of Burkitt's lymphoma." However, recently, Niller and colleagues proposed a new model for the development of Burkitt's lymphoma.² In their model, a central role is played by the EBV-encoded RNA (EBER) locus of the EBV genome, the product of which has been implicated in EBV-related tumorigenesis, mainly by inhibiting apoptosis.³ The authors based their hypothesis on a binding site for c-Myc . . . [Full Text of this Article]

HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  TERMS OF USE  |  HELP  |  beta.nejm.org Comments and questions? Please contact us. The New England Journal of Medicine is owned, published, and copyrighted © 2009 Massachusetts Medical Society. All rights reserved.