RIPK3 Restricts Myeloid Leukemogenesis by Promoting Cell Death and Differentiation of Leukemia Initiating Cells.

Höckendorf, Ulrike; Yabal, Monica; Herold, Tobias; Munkhbaatar, Enkhtsetseg; Rott, Stephanie; Jilg, Stefanie; Kauschinger, Johanna; Magnani, Giovanni; Reisinger, Florian; Heuser, Michael; Kreipe, Hans; Sotlar, Karl; Engleitner, Thomas; Rad, Roland; Weichert, Wilko; Peschel, Christian; Ruland, Jürgen; Heikenwalder, Mathias; Spiekermann, Karsten; Slotta-Huspenina, Julia; Groß, Olaf; Jost, Philipp J

doi:10.1016/j.ccell.2016.06.002

Benutzer: Gast

journal article

Dokumenttyp:: journal article
Autor(en):: Höckendorf, Ulrike; Yabal, Monica; Herold, Tobias; Munkhbaatar, Enkhtsetseg; Rott, Stephanie; Jilg, Stefanie; Kauschinger, Johanna; Magnani, Giovanni; Reisinger, Florian; Heuser, Michael; Kreipe, Hans; Sotlar, Karl; Engleitner, Thomas; Rad, Roland; Weichert, Wilko; Peschel, Christian; Ruland, Jürgen; Heikenwalder, Mathias; Spiekermann, Karsten; Slotta-Huspenina, Julia; Groß, Olaf; Jost, Philipp J
Titel:: RIPK3 Restricts Myeloid Leukemogenesis by Promoting Cell Death and Differentiation of Leukemia Initiating Cells.
Abstract:: 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-1? 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. «
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(-... »
Zeitschriftentitel:: Cancer Cell
Jahr:: 2016
Band / Volume:: 30
Heft / Issue:: 1
Seitenangaben Beitrag:: 75-91
Sprache:: eng
Volltext / DOI:: doi:10.1016/j.ccell.2016.06.002
PubMed:: http://view.ncbi.nlm.nih.gov/pubmed/27411587
Print-ISSN:: 1535-6108
TUM Einrichtung:: Institut für Allgemeine Pathologie und pathologische Anatomie
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mediaTUM Gesamtbestand Einrichtungen Schools TUM School of Medicine and Health Departments Preclinical Medicine Institut für Allgemeine Pathologie und Pathologische Anatomie (Dr. Mogler komm.)2016

mediaTUM Gesamtbestand Hochschulbibliographie 2016 Fakultäten Medizin Institut für Allgemeine Pathologie und Pathologische Anatomie