Walking the Tightrope: Balancing Delicate Inflammation Response to Eradicate Acute Myeloid Leukemia.
Alexandre PuissantHind MedyoufPublished in: Cancer discovery (2022)
Ellegast and colleagues show that monocytic acute myeloid leukemias (AML), enriched in inflammatory and immune gene sets, exploit a transcriptional repressor-namely, IRF2BP2-to mitigate their cell-intrinsic inflammatory output and ensure their maintenance. IRF2BP2 ablation results in heightened inflammatory signals that reach a set point that triggers apoptotic AML cell death in an NF-κB-IL1β-dependent manner. The study identifies IRF2BP2 as a cell-intrinsic vulnerability with potential therapeutic significance in monocytic AML. See related article by Ellegast et al., p. 1760 (6).
Keyphrases
- acute myeloid leukemia
- cell death
- oxidative stress
- allogeneic hematopoietic stem cell transplantation
- dendritic cells
- single cell
- cell therapy
- genome wide
- signaling pathway
- liver failure
- gene expression
- climate change
- copy number
- transcription factor
- dna methylation
- acute lymphoblastic leukemia
- bone marrow
- cell cycle arrest
- lps induced
- pi k akt
- toll like receptor