Cooperation of cancer drivers with regulatory germline variants shapes clinical outcomes

Interactions between germline variants and somatic mutations is a relatively unexplored topic in cancer. Here, in Ewing sarcoma, the authors show that binding of the oncogenic EWSR1-FLI1 fusion transcription factor to a polymorphic enhancer-like DNA element controls MYBL2, whose high expression corr...

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Autores principales: Julian Musa, Florencia Cidre-Aranaz, Marie-Ming Aynaud, Martin F. Orth, Maximilian M. L. Knott, Olivier Mirabeau, Gal Mazor, Mor Varon, Tilman L. B. Hölting, Sandrine Grossetête, Moritz Gartlgruber, Didier Surdez, Julia S. Gerke, Shunya Ohmura, Aruna Marchetto, Marlene Dallmayer, Michaela C. Baldauf, Stefanie Stein, Giuseppina Sannino, Jing Li, Laura Romero-Pérez, Frank Westermann, Wolfgang Hartmann, Uta Dirksen, Melissa Gymrek, Nathaniel D. Anderson, Adam Shlien, Barak Rotblat, Thomas Kirchner, Olivier Delattre, Thomas G. P. Grünewald
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2019
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Acceso en línea:https://doaj.org/article/b15283577e6941feafb9a8d8c4019ddd
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Sumario:Interactions between germline variants and somatic mutations is a relatively unexplored topic in cancer. Here, in Ewing sarcoma, the authors show that binding of the oncogenic EWSR1-FLI1 fusion transcription factor to a polymorphic enhancer-like DNA element controls MYBL2, whose high expression correlates with prognosis.