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Abstract
Patients with acute lymphoblastic leukemia (ALL) often face relapse and death due to chemoresistance to standard chemotherapy treatment. Based on studies that have evaluated benfotiamine’s anticancer properties, BFO increases intracellular thiamine pyrophosphate (TPP) levels and compromises cancer cell viability. Cancer cell metabolism is dependent on endogenous TPP, and it would not be anticipated that thiamine uptake and subsequent TPP formation would be susceptible to acquired or intrinsic chemoresistance mechanisms. Therefore, we hypothesize that benfotiamine will produce similar anticancer activity in chemoresistant cancer cells as in wildtype acute lymphoblastic leukemia. The results of this study showed that twice the dose of BFO was required to compromise cell viability in the chemoresistant ALL cell line, as compared to the chemo-naïve parental line. Therefore, there is great therapeutic potential for higher concentrations of benfotiamine to be employed in the treatment of chemoresistant cancers.