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Inhibition of the NADPH oxidase regulates heme oxygenase 1 expression in chronic myeloid leukemia

Patients with chronic myelogenous leukemia (CML) in blast crisis have a poor response to tyrosine kinase inhibitors designed to inhibit the breakpoint cluster region–v‐Abelson murine leukemia viral oncogene homolog 1 (BCR‐ABL1) oncogene. Recent work has demonstrated that heme oxygenase 1 (HO‐1) expression is increased in BCR‐ABL1–expressing cells and that the inhibition of HO‐1 in CML leads to reduced cellular growth, suggesting that HO‐1 may be a plausible target for therapy. The objective of the current study was to clarify the mechanism of HO‐1 overexpression and the role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase as a contributor to this mechanism in CML.