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ABSTRACT
This commentary highlights a pivotal study revealing the dual role of heme metabolism in acute myeloid leukemia (AML). It discusses how AML cells, residing in a low-heme level to maintain stemness, become uniquely vulnerable to further inhibition of heme biosynthesis, which triggers mitochondrial complex IV disassembly and induces cuproptosis. Furthermore, the review underscores co-inhibition of heme synthesis and glycolysis as a synthetic lethal strategy that exploits a unique metabolic liability in AML.-
Keywords:
- Target therapy /
- Heme metabolism /
- Hematologic malignancies
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ABOUT THIS ARTICLE
Cite this article:
Xintong Deng, Yu Liu, Lanxin Zhang, Jianan Zheng, Wanyue Zhou, Chong Chen. Targeting heme biosynthesis in acute myeloid leukemia[J]. The Innovation Medicine. https://doi.org/10.59717/j.xinn-med.2027.100283
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Xintong Deng, Yu Liu, Lanxin Zhang, Jianan Zheng, Wanyue Zhou, Chong Chen. Targeting heme biosynthesis in acute myeloid leukemia[J]. The Innovation Medicine. https://doi.org/10.59717/j.xinn-med.2027.100283
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