Abstract
The present study reports the potential of furosemide therapeutic activity in acute myeloid leukemia. A 26-year-old man with acute biphenotypic leukemia was treated with furosemide for suspected pulmonary edema, which was later deemed to be an infiltration of leukemia cells. Notably, the myeloblast population was rapidly eliminated during furosemide therapy. Bone marrow specimens biopsied at different time points were used for immunohistochemical analysis of the expression levels of tumor necrosis factor-α (TNF-α) and its two receptors, TNF-α receptors 1 and 2. The expression of TNF-α and its receptors in the bone marrow was markedly suppressed by furosemide, along with the elimination of the myeloblasts. Thus, it was hypothesized that the growth of myeloblasts in the patient depended on autocrine and/or paracrine TNF-α stimulation, whereas furosemide disrupted this positive feedback loop. Therefore, furosemide is suggested as an effective therapeutic agent for acute myeloid leukemia, at least as an adjunct to standard chemotherapy and gene-targeted therapy.