Université Paris Cité, Génomes, Biologie Cellulaire et Thérapeutique U944, INSERM, CNRS, Paris, France.
Georg-Speyer-Haus, Institute for Tumor Biology and Experimental Therapy, Frankfurt am Main, Germany.
Cancer Discov. 2022 Jul 6;12(7):1617-1619. doi: 10.1158/2159-8290.CD-22-0473.
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).
埃尔莱加斯特及其同事表明，富含炎症和免疫基因集的单核细胞性急性髓系白血病 (AML) 利用转录抑制剂——IRF2BP2——来减轻其内在的炎症输出并确保其自身的维持。IRF2BP2 的缺失会导致炎症信号升高，达到一个临界点，从而以 NF-κB-IL1β 依赖的方式触发凋亡性 AML 细胞死亡。该研究鉴定出 IRF2BP2 是单核细胞性 AML 中的一种内在脆弱性，具有潜在的治疗意义。见埃尔莱加斯特等人的相关文章，第 1760 页（6）。
