{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T19:28:06Z","timestamp":1791228486271,"version":"4.1.0"},"reference-count":57,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2007,1,8]],"date-time":"2007-01-08T00:00:00Z","timestamp":1168214400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2007,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Deregulation of the proto\u2010oncogene <jats:italic>c\u2010myc<\/jats:italic> is a key event in the pathogenesis of many tumors. A paradigm is the activation of the <jats:italic>c\u2010myc<\/jats:italic> gene by chromosomal translocations in Burkitt lymphoma (BL). Despite expression of a restricted set of Epstein\u2013Barr viral (EBV) antigens, BL cells are not recognized by antigen\u2010specific cytotoxic T cells (CTLs) because of their inability to process and present HLA class I\u2010restricted antigens. In contrast, cells of EBV\u2010driven posttransplant lymphoproliferative disease (PTLD) are recognized and rejected by EBV\u2010specific CTLs. It is not known whether the poor immunogenicity of BL cells is due to nonexpression of viral antigens, overexpression of c\u2010myc, or both. To understand the basis for immune recognition and escape, we have compared the mRNA expression profiles of BL and EBV\u2010immortalized cells (as PTLD model). Among the genes expressed at low level in BL cells, we have identified many genes involved in the NF\u2010\u03baB and interferon response that play a pivotal role in antigen presentation and immune recognition. Using a cell line in which EBNA2 and c\u2010myc can be regulated at will, we show that c\u2010MYC negatively regulates STAT1, the central player linking the Type\u2010I and Type\u2010II interferon response. Switching off <jats:italic>c\u2010myc<\/jats:italic> expression leads to STAT1 induction through a direct and indirect mechanism involving induction of Type\u2010I interferons. c\u2010MYC thus masks an interferon\u2010inducing activity in these cells. Our findings imply that immune escape of tumor cells is not only a matter of <jats:italic>in vivo<\/jats:italic> selection but may be additionally promoted by activation of a cellular oncogene. \u00a9 2007 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ijc.22372","type":"journal-article","created":{"date-parts":[[2007,1,8]],"date-time":"2007-01-08T21:47:31Z","timestamp":1168292851000},"page":"1387-1395","source":"Crossref","is-referenced-by-count":87,"title":["c\u2010MYC activation impairs the NF\u2010\u03baB and the interferon response: Implications for the pathogenesis of Burkitt's 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