Jul 2026· Human Cell· Vol 39· 0 citations· 38 references
Medicine
TL;DR
SLC25A51 represents a promising metabolic target with potential to overcome therapeutic resistance and improve patient outcomes in AML, and its potential implications across distinct genetic subtypes of AML are discussed, thereby highlighting key directions for future translational research.
Background/Objectives: Chronic myeloid leukemia (CML) is a hematopoietic stem cell malignancy initiated by the BCR::ABL1 oncoprotein. Although tyrosine kinase inhibitors (TKIs) have revolutionized CML therapy, resistance remains a major clinical challenge. Emerging evidence suggests that metabolic reprogramming contrib...
Ezzahra Rachid, M. Lahmouad, Rawane Bellemrrabet et al.· Biomedicines· 0 citations
Acute myeloid leukemia (AML) cells rely heavily on mitochondrial oxidative phosphorylation (OXPHOS) for energy, making mitochondrial function a promising therapeutic target. TCF12, a transcription factor belonging to the basic helix-loop-helix (bHLH) family, has been implicated in various cancers and is highly expresse...
Findings establish Malonyl-CoA:ACP transacylase (MCAT), a Lauren subtype-associated gene encoding a key mitochondrial fatty acid synthesis (mtFAS) enzyme, as a metabolic switch that links ROS/P53-dependent cell death and therapeutic target for GC.
Yu-Fei Wang, Meng Zhu, Xin Yin et al.· Cell Death and Differentiati...· 0 citations
In conclusion, AR-V7-driven mitochondrial metabolic remodeling is central to enzalutamide resistance; future studies should dissect AR-V7–mitochondria regulatory nodes and optimize mitochondria-targeted combination strategies.
Rong-Xin Chang, Zhuang-Zhuang Zhang· Serican Journal of Medicine· 0 citations
PTBP1 is established as a critical regulator of AML cell fitness and a clinically actionable therapeutic combination that exploits AML dependency on PTBP1-CDC42 signaling to enhance the efficacy of venetoclax-based regimens is identified.
