Unleashing Cell-Intrinsic Inflammation as a Strategy to Kill AML Blasts.
Jana M EllegastGabriela AlexeAmanda HamzeShan LinHannah J UckelmannPhilipp J RauchMaxim PimkinLinda S RossNeekesh V DhariaAmanda L RobichaudAmy Saur ConwayDelan KhalidJennifer A PerryMark WunderlichLina BenajibaYana PikmanBehnam NabetNathanael S GrayStuart H OrkinKimberly StegmaierPublished in: Cancer discovery (2022)
This study exploits inflammatory programs inherent to AML blasts to identify genetic vulnerabilities in this disease. In doing so, we determined that AML cells are dependent on the transcriptional repressive activity of IRF2BP2 for their survival, revealing cell-intrinsic inflammation as a mechanism priming leukemic blasts for regulated cell death. See related commentary by Puissant and Medyouf, p. 1617. This article is highlighted in the In This Issue feature, p. 1599.
Keyphrases
- acute myeloid leukemia
- oxidative stress
- cell death
- single cell
- cell cycle arrest
- induced apoptosis
- cell therapy
- allogeneic hematopoietic stem cell transplantation
- transcription factor
- public health
- machine learning
- dendritic cells
- mesenchymal stem cells
- acute lymphoblastic leukemia
- signaling pathway
- cell proliferation
- immune response
- free survival
- neural network