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F. Diop et al.
Non-canonical NF-κB activation by BIRC3 mutations bypasses the block of BTK by ibrutinib. Consistently, NF- κB activation and cell survival are unaffected by ibrutinib in both CLL cells (our study) and mantle cell lymphoma cells.14 If this preclinical evidence is validated in ibrutinib- treated patients, BIRC3 mutations may also translate into a biomarker for informing selection of novel agents.
Acknowledgments
This work was supported by: Molecular bases of disease dis- semination in lymphoid malignancies to optimize curative thera- peutic strategies, (5 x 1000 n. 21198), Associazione Italiana per la Ricerca sul Cancro Foundation, Milan, Italy (grants to GG and RF) and Progetti di Rilevante Interesse Nazionale (PRIN),
(2015ZMRFEA), Rome, Italy; partially funded by the AGING Project – Department of Excellence – DIMET, Università del Piemonte Orientale, Novara, Italy; partially funded by Novara AIL ONLUS, Novara, Italy; Associazione Italiana per la Ricerca sul Cancro (AIRC IG-17314); Swiss Cancer League, ID HSR- 4660-11-2018, Bern, Switzerland; Research Advisory Board of the Ente Ospedaliero Cantonale, Bellinzona, Switzerland; European Research Council (ERC) Consolidator grant CLL- CLONE ID: 772051; grant n. 320030_169670/1 Swiss National Science Foundation, Berne, Switzerland; Fondazione Fidinam, Lugano, Switzerland; Nelia & Amadeo Barletta Foundation, Lausanne, Switzerland; Fond’Action, Lausanne, Switzerland; Translational Research Program, grant n. 6594-20, The Leukemia & Lymphoma Society, New York, USA.
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