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Thus, either <jats:styled-content style=\"fixed-case\">DLBCL<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">FL<\/jats:styled-content> can give rise to aggressive double\u2010hit lymphomas (<jats:styled-content style=\"fixed-case\">DHL<\/jats:styled-content>) with concurrent activation of <jats:italic><jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content><\/jats:italic> and <jats:italic><jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>2<\/jats:italic>. Research over the last three decades has improved our understanding of the functions of these oncogenes and the basis for their cooperative action in lymphomagenesis. <jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content>, in particular, is a transcription factor that contributes to cell activation, growth and proliferation, while concomitantly sensitizing cells to apoptosis, the latter being blocked by <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>2. Here, we review our current knowledge about the role of <jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content> in germinal center B\u2010cells and lymphomas, discuss <jats:styled-content style=\"fixed-case\">MYC<\/jats:styled-content>\u2010induced dependencies that can sensitize cancer cells to select pharmacological inhibitors, and illustrate their therapeutic potential in aggressive lymphomas\u2014and in particular in <jats:styled-content style=\"fixed-case\">DHL<\/jats:styled-content>, in combination with <jats:styled-content style=\"fixed-case\">BCL<\/jats:styled-content>2 inhibitors.<\/jats:p>","DOI":"10.1111\/imr.12734","type":"journal-article","created":{"date-parts":[[2019,3,15]],"date-time":"2019-03-15T09:06:39Z","timestamp":1552640799000},"page":"178-197","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["<scp>MYC<\/scp> in Germinal Center\u2010derived lymphomas: Mechanisms and therapeutic 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