Burkitt lymphoma and diffuse large B-cell lymphoma (DLBCL) are both non-Hodgkin lymphomas of B-cells that share features such as hyperactivation of the MYC oncogene due to translocation events, but the other genetic events that are shared between these diseases are not fully understood. Gong and colleagues showed that DDX3X loss-of-function mutations, which disrupt the function of an important RNA helicase, were recurrent in both Burkitt lymphoma as well as in MYC-driven DLBCL. The authors then investigated the significance of DDX3X mutations in both early lymphoma development and after tumors were established. Initially, loss of DDX3X is protective against MYC-induced stress by limiting translation and protein synthesis, and unexpectedly, the authors observed that fully transformed lymphoma cells upregulate expression of the DDX3X homolog DDX3Y in order to restore full capacity of the translation machinery.

Expert Commentary: This study proposes an appealing approach for treatment of MYC-driven lymphoma based on compounds either...

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