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c-MYC activation impairs the NF-kappa B and the interferon response: Implications for the pathogenesis of Burkitt's lymphoma
dc.creator | Schlee, Martin | |
dc.creator | Hoelzel, Michael | |
dc.creator | Bernard, Sandra | |
dc.creator | Mailhammer, Reinhard | |
dc.creator | Schuhmacher, Marino | |
dc.creator | Reschke, Judith | |
dc.creator | Eick, Dirk | |
dc.creator | Marinković, Dragan | |
dc.creator | Wirth, Thomas | |
dc.creator | Rosenwald, Andreas | |
dc.creator | Staudt, Louis M. | |
dc.creator | Eilers, Martin | |
dc.creator | Baran-Marszak, Fanny | |
dc.creator | Fagard, Remi | |
dc.creator | Feuillard, Jean | |
dc.creator | Laux, Gerhard | |
dc.creator | Bornkamm, Georg W. | |
dc.date.accessioned | 2021-06-09T13:17:46Z | |
dc.date.available | 2021-06-09T13:17:46Z | |
dc.date.issued | 2007 | |
dc.identifier.issn | 0020-7136 | |
dc.identifier.uri | http://rfasper.fasper.bg.ac.rs/handle/123456789/119 | |
dc.description.abstract | Deregulation of the proto-oncogene c-myc is a key event in the pathogenesis of many tumors. A paradigm is the activation of the c-myc gene by chromosomal translocations in Burkitt lymphoma (BL). Despite expression of a restricted set of Epstein-Barr viral (EBV) antigens, BL cells are not recognized by antigen-specific cytotoxic T cells (CTLs) because of their inability to process and present HLA class I-restricted antigens. In contrast, cells of EBV-driven posttransplant lymphoproliferative disease (PTLD) are recognized and rejected by EBV-specific CTLs. It is not known whether the poor immunogenicity of BL cells is due to nonexpression of viral antigens, overexpression of c-myc, or both. To understand the basis for immune recognition and escape, we have compared the mRNA expression profiles of BL and EBV-immortalized cells (as PTLD model). Among the genes expressed at low level in BL cells, we have identified many genes involved in the NF-kappa B and interferon response that play a pivotal role in antigen presentation and immune recognition. Using a cell line in which EBNA2 and c-myc can be regulated at will, we show that c-MYC negatively regulates STAT1, the central player linking the Type-I and Type-H interferon response. Switching off c-myc expression leads to STAT1 induction through a direct and indirect mechanism involving induction of Type-I interferons. c-MYC thus masks an interferon-inducing activity in these cells. Our findings imply that immune escape of tumor cells is not only a matter of in vivo selection but may be additionally promoted by activation of a cellular oncogene. | en |
dc.publisher | Wiley-Liss, Hoboken | |
dc.relation | Intramural NIH HHSUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA Funding Source: Medline | |
dc.rights | openAccess | |
dc.source | International Journal of Cancer | |
dc.subject | Burkitt's lymphoma | en |
dc.subject | c-myc | en |
dc.subject | STAT1 | en |
dc.subject | interferon | en |
dc.subject | NF-kappa B | en |
dc.subject | antigen presentation | en |
dc.title | c-MYC activation impairs the NF-kappa B and the interferon response: Implications for the pathogenesis of Burkitt's lymphoma | en |
dc.type | article | |
dc.rights.license | ARR | |
dc.citation.epage | 1395 | |
dc.citation.issue | 7 | |
dc.citation.other | 120(7): 1387-1395 | |
dc.citation.rank | M21 | |
dc.citation.spage | 1387 | |
dc.citation.volume | 120 | |
dc.identifier.doi | 10.1002/ijc.22372 | |
dc.identifier.pmid | 17211884 | |
dc.identifier.scopus | 2-s2.0-33847662881 | |
dc.identifier.wos | 000244610700002 | |
dc.type.version | publishedVersion |
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