Abstract
The dietary consumption of fructose has increased in the last five decades, paralleled by an increase in obesity. Excess fructose intake is linked to obesity, metabolic syndrome, non-alcoholic fatty liver disease, diabetes, hypertension, cardiac disease, and several aggressive types of cancer. The incidence of acute myeloid leukemia (AML), a lethal hematologic malignancy, has also increased in parallel. Despite significant advances in our understanding of AML, including molecular genetics and more effective targeted therapies, relapse is frequent and outcomes remain poor. Moreover, except for several known causes for a small proportion of AML cases, virtually nothing is known about the initial causative leukemogenic event. In this study, the author asked and intended to answer the question, “can excess fructose intake lead to the initial cellular event that causes AML?” The author reviewed published literature to answer the above question and, subsequently, to identify novel AML therapies based on fructose metabolism. In this article, fructose metabolism and its relationship with metabolic pathways essential for AML, including regulation by hypoxia inducible factor, are described. Evidence for the potential etiologic role of fructose in AML is summarized for the first time. To conclude, excess fructose can lead to the initial AML-causative cellular event. Based on this study, future studies are warranted to determine if restricting fructose intake can prevent AML. Therapeutically, the development of hypoxia inducible factor and glucose transporter 5 inhibitors should be pursued for the treatment of AML.
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