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RIPK3 restricts myeloid leukemogenesis by promoting cell death and differentiation of leukemia initiating cells.
Cancer Cell 30, 75-91 (2016)
Publ. Version/Full Text
DOI
PMC
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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Publication type
Article: Journal article
Document type
Scientific Article
Keywords
Nlrp3 Inflammasome Activation; Hematopoietic Stem; Progenitor Cells; In-vitro; Necrosis; Mice; Mlkl; Aml; Necroptosis; Mutations
ISSN (print) / ISBN
1535-6108
e-ISSN
1878-3686
Journal
Cancer Cell
Quellenangaben
Volume: 30,
Issue: 1,
Pages: 75-91
Publisher
Cell Press
Publishing Place
Cambridge, Mass.
Non-patent literature
Publications
Reviewing status
Peer reviewed
Institute(s)
Institute of Virology (VIRO)