Exploring FLT3 driven acute myeloid leukemia for novel immunotherapeutic options.

Abstract

Acute myeloid leukemia (AML) is one of the subtypes of leukemia that is genetically and medically heterogeneous. The FLT3-ITD mutant variant is one of its form of leukemia, that constitutes 30% of the occurrences. This mutation confers inferior prognosis. This could be due to several reasons, one of them being immune evasion. In an effort to unravel how this evasion happens, we hypothesize that FLT3-ITD mutation could be causing the upregulation of PD-L1. PD-L1 have immunosuppressive roles in immune response to certain types of cancers. Using Flow cytometry, PD-L1 surface expression was observed on the murine model cell line Ba/F3, transfected with plasmids encoding human wild type FLT3, and the FLT3-ITD mutation. PD-L1 was up regulated in both FLT3 and FLT3-ITD Ba/F3 cells. Yet, this was not the case for the human cell line MV4-11, both using flow cytometry and western blot. We conclude that FLT3-ITD is not upregulating PD-L1 in this AML cell type. Regardless, the results obtained in the murine model suggest that more experiments are needed to understand the role of FLT3 in the regulation of PD-L1 levels.