Publications by authors named "S Mouche"
Article Synopsis
- Acute myeloid leukemia (AML) is a difficult-to-treat blood cancer, mainly due to the presence of leukemic stem cells (LSCs) that lead to treatment resistance and relapse.
- This research focuses on how the quiescence (dormancy) of LSCs and related molecular mechanisms impact AML development, revealing that quiescent LSCs have a distinct gene signature and increased autophagic activity that helps them survive.
- The study identifies nuclear receptor coactivator 4 (NCOA4) as a key player in iron metabolism for quiescent LSCs, showing that inhibiting NCOA4 can effectively target these cells without harming normal blood progenitors, highlighting its potential as
Article Synopsis
- The study explores the role of the transcription factor CCAAT-enhancer binding protein α (C/EBPα) in lipid metabolism and cellular homeostasis in acute myeloid leukemia (AML), particularly with mutations in FLT3.
- Researchers found that C/EBPα and FLT3 activation enhance lipid production and desaturation in AML cells, leading to increased vulnerability to oxidative stress.
- Inhibiting C/EBPα or FLT3 demonstrates potential for therapeutic strategies targeting lipid metabolism to promote ferroptotic cell death in FLT3-mutant AML, a type of leukemia affecting 30% of patients.
Article Synopsis
- Mitochondrial metabolism is crucial for acute myeloid leukemia (AML) and is regulated by proteins that manage mitochondrial shape through fusion and fission processes.*
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- Research indicates that targeting mitochondrial fusion presents a new vulnerability in AML cells, demonstrated through studies using patient-derived xenograft (PDX) models.*
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- Disruption of mitochondrial fusion through genetic depletion or pharmacological inhibition significantly impairs AML cell growth by affecting respiration and causing cell cycle arrest, suggesting a potential therapeutic strategy.*
