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Höckendorf, U.* ; Yabal, M.* ; Herold, T.* ; Munkhbaatar, E.* ; Rott, S.* ; Jilg, S.* ; Kauschinger, J.* ; Magnani, G.* ; Reisinger, F. ; Heuser, M.* ; Kreipe, H.* ; Sotlar, K.* ; Engleitner, T.* ; Rad, R.* ; Weichert, W.* ; Peschel, C.* ; Ruland, J.* ; Heikenwälder, M. ; Spiekermann, K.* ; Slotta-Huspenina, J.* ; Groß, O.* ; Jost, P.J.*

RIPK3 restricts myeloid leukemogenesis by promoting cell death and differentiation of leukemia initiating cells.

Cancer Cell 30, 75-91 (2016)

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Since acute myeloid leukemia (AML) is characterized by the blockade of hematopoietic differentiation and cell death, we interrogated RIPK3 signaling in AML development. Genetic loss of Ripk3 converted murine FLT3-ITD-driven myeloproliferation into an overt AML by enhancing the accumulation of leukemia-initiating cells (LIC). Failed inflammasome activation and cell death mediated by tumor necrosis factor receptor caused this accumulation of LIC exemplified by accelerated leukemia onset in Il1r1(-/-), Pycard(-/-), and Tnfr1/2(-/-) mice. RIPK3 signaling was partly mediated by mixed lineage kinase domain-like. This link between suppression of RIPK3, failed interleukin-1β release, and blocked cell death was supported by significantly reduced RIPK3 in primary AML patient cohorts. Our data identify RIPK3 and the inflammasome as key tumor suppressors in AML.

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