Inhibition of NLRP3 enhances pro-apoptotic effects of FLT3 inhibition in AML.
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ABSTRACT: FLT3 mutations occur in approximately 25% of all acute myeloid leukemia (AML) patients. While several FLT3 inhibitors have received FDA approval, their use is currently limited to combination therapies with chemotherapy, as resistance occurs, and efficacy decreases when the inhibitors are used alone. Given the highly heterogeneous nature of AML, there is an urgent need for novel targeted therapies that address the disease from multiple angles. Recent research has identified the NLRP3 inflammasome as a potential new driver in AML. Here, we investigated the efficacy of different NLRP3 inhibitors in targeting AML cells in vitro. Our findings reveal that NLRP3 inhibition induces cell cycle arrest as well as signs of senescence in multiple AML cell lines. In contrast, NLRP3 inhibition selective
SUBMITTER: Sieberer H
PROVIDER: S-EPMC11773904 | biostudies-literature | 2025 Jan
REPOSITORIES: biostudies-literature
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