Abstract
Background Acute myeloid leukemia (AML) accounts for 15-20% of childhood leukemias. Although remission is achieved following treatment with front-line chemotherapy, nearly half of the patients are faced with disease relapse associated with chemoresistance. Therefore, therapies that could sustain the remission phase in pediatric AML are urgently needed. Metformin is a widely used antidiabetic drug known to exhibit anti-cancer effect in several malignancies. Metformin is well-tolerated at very high doses, and its safety has also been demonstrated in clinical trials in diabetic children.
Highlights
Acute myeloid leukemia (AML) accounts for 15-20% of childhood leukemias
Cells were stained with Annexin V-FITC and apoptotic cells were detected by flow cytometry
Low doses of metformin (0.5 mM) resulted in suppression of colony formation in a clonogenicity assay. In correlation with this data, we observed that low dose metformin treated cells exhibited delayed engraftment in an AML xenograft mouse model with 50% reduction in the percentage of AML cells in mouse blood
Summary
Acute myeloid leukemia (AML) accounts for 15-20% of childhood leukemias. Remission is achieved following treatment with front-line chemotherapy, nearly half of the patients are faced with disease relapse associated with chemoresistance. Therapies that could sustain the remission phase in pediatric AML are urgently needed. Metformin is a widely used antidiabetic drug known to exhibit anti-cancer effect in several malignancies. Metformin is well-tolerated at very high doses, and its safety has been demonstrated in clinical trials in diabetic children
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