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Paradigm shift: combination BET and JAK inhibition in myelofibrosis

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Fig. 1: Inhibitors targeting Janus Associated Kinase 2 (JAK2) and bromodomain and extraterminal domain (BET) proteins cooperate to downregulate NFκB activity as well as expression of target genes that contribute to the underlying pathologic features of myelofibrosis.

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Acknowledgements

JM, AG, and SV conceived the work that led to the submission, drafted the paper, approved the final version, and agreed to be accountable for all aspects of the work.

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Correspondence to John Mascarenhas.

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JM has received research support paid to his institution from PharmaEssentia, Abbvie, CTI Bio, Merck, Roche, Novartis, BMS, Forbius, Kartos, Incyte, Geron, Sierra Oncology; consulting or advisory board fees from Kartos, CTI Bio, Constellation, Incyte, Roche, Novartis, BMS, Abbvie, PharmaEssentia, and Geron. AG has received advisory board fees from PharmaEssentia, BMS, Novartis, AbbVie, Sierra Oncology. SV has received research support paid to his institution from Incyte, Roche, NS Pharma, Celgene, Gilead, Promedior, CTI BioPharma, Blueprint Medicines Corp., Novartis, Sierra Oncology, PharmaEssentia, Constellation, Protagonist, Kartos; advisory board fees from Constellation, BMS, Sierra Oncology, Incyte, Novartis, Celgene, PharmaEssentia.

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Mascarenhas, J., Gerds, A. & Verstovsek, S. Paradigm shift: combination BET and JAK inhibition in myelofibrosis. Leukemia (2021). https://doi.org/10.1038/s41375-021-01405-z

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