In vivo ablation of NFκB cascade effectors alleviates disease burden in myeloproliferative neoplasms

Hyperactivation of the NFκB cascade propagates oncogenic signaling and pro-inflammation, which together augments disease burden in myeloproliferative neoplasms (MPNs). Here, we systematically ablate NFκB signaling effectors to identify core dependencies using a series of primary samples and syngeneic and patient-derived xenograft (PDX) mouse models. Conditional knockout of Rela attenuated Jak2V617F and MPLW515L-driven onset of polycythemia vera and myelofibrosis disease hallmarks, …