CD52 is a novel target for the treatment of FLT3-ITD-mutated myeloid leukemia.

ABSTRACT: Internal tandem duplication (ITD) of FMS-like tyrosine kinase 3 (FLT3) confers poor prognosis and is found in approximately 25% of cases of acute myeloid leukemia (AML). Although FLT3 inhibitors have shown clinical benefit in patients with AML harboring FLT3-ITD, the therapeutic effect is limited. Here, to explore alternative therapeutics, we established a cellular model of monoallelic FLT3^ITD/WT cells using the CRISPR-Cas9 system in a human myeloid leukemia cell line, K562. cDNA microarray analysis revealed elevated CD52 expression in K562-FLT3^ITD/WT cells compared to K562-FLT3^WT/WT cells, an observation that was further confirmed by quantitative real-time-PCR and flow cytometric analyses. The elevated expression of CD52 in K562-FLT3^ITD/WT cells

SUBMITTER: Karnan S 

PROVIDER: S-EPMC8149417 | biostudies-literature | 2021 May

REPOSITORIES: biostudies-literature