fig2

Targeting metabolic vulnerabilities to overcome resistance to therapy in acute myeloid leukemia

Figure 2. Overview of cellular metabolic pathways and their crosstalk -including: (1) glycolysis; (2) TCA cycle; (3) OXPHOS; (4) glutaminolysis; (5) nucleic acid biosynthesis; (6) lipid synthesis; (7) fatty acid import and oxidation; (8) ROS mitigation by GSH; (9) ferroptosis. ACC: Ac-CoA carboxylase; ACLY: ATP citrate lyase; ADP: adenosine diphosphate; ATP: denosine triphosphate; α-KG: α-ketoglutarate; CAT: carnitine acetyltransferase; CPT1: carnitine palmitoyltransferase 1; CPT2: carnitine palmitoyltransferase 2; DHO: dihydroorotate; DHODH: dihydroorotate dehydrogenase; FAD: flavin adenine dinucleotide; FASN: FA synthase; GSH: glutathione; IDH: isocitrate dehydrogenase enzyme; GCL: glutamate-cysteine ligase; GSS: glutathione synthetase; GLS1: glutaminase 1; NAD: nicotinamide adenine dinucleotide; NADH: nicotinamide adenine dinucleotide (NAD) + hydrogen (H); MUFA: monounsaturated fatty acid; OXPHOS: oxidative phosphorylation; PUFA: polyunsaturated fatty acid; ROS: reactive oxygen species; TCA: tricarboxylic acid cycle; UMP: uridine monophosphate.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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