{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,12]],"date-time":"2025-11-12T20:39:05Z","timestamp":1762979945357,"version":"build-2065373602"},"reference-count":36,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2013,2,22]],"date-time":"2013-02-22T00:00:00Z","timestamp":1361491200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["pathsocjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Pathology"],"published-print":{"date-parts":[[2013,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:bold>Burkitt lymphoma (<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>) is caused by translocation of the <jats:italic><jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content><\/jats:italic> gene to an immunoglobulin locus resulting in its constitutive expression depending on the activity of the immunoglobulin (Ig) enhancer elements. Treatment of <jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content> cell lines with epigenetic modifiers is known to repress B\u2010cell\u2010specific genes and to up\u2010regulate B\u2010cell\u2010inappropriate genes including the transcription repressor <jats:styled-content style=\"fixed-case\">ID2<\/jats:styled-content> expression. We found that the <jats:styled-content style=\"fixed-case\">DNA<\/jats:styled-content> methyltransferase inhibitor decitabine\/5\u2010aza\u20102\u2010deoxycytidine (5\u2010aza\u2010<jats:styled-content style=\"fixed-case\">dC<\/jats:styled-content>) represses the <jats:italic><jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content><\/jats:italic> oncogene on <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> and protein levels by inducing <jats:styled-content style=\"fixed-case\">ID2<\/jats:styled-content>. Down\u2010regulation of <jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content> was associated with repression of transcriptional activity of the Ig locus and with inhibition of proliferation. The induction of <jats:styled-content style=\"fixed-case\">ID2<\/jats:styled-content> can be in part explained by activation of the transcription factor <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB. We conclude that up\u2010regulation of <jats:styled-content style=\"fixed-case\">ID2<\/jats:styled-content> contributes to anti\u2010tumour activity of 5\u2010aza\u2010<jats:styled-content style=\"fixed-case\">dC<\/jats:styled-content> via repression of Ig locus activity and consequently <jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content> expression. Copyright \u00a9 2013 Pathological Society of Great Britain and Ireland. 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