Abstract
MLAA-34 is a newly identified monocytic leukemia-associated antigen that is overexpressed in acute monocytic leukemia specifically, thus providing a novel target for the therapy of acute monocytic leukemia. In this study, we first expressed MLAA-34 protein in Escherichia coli (E.coli) BL21 (DE3) cells and purified it by nickel ion affinity chromatography with high purity (>90%). Then, MLAA-34 was used as antigen for biopanning anti-MLAA-34 single chain antibody fragment (ScFv) from a fully human ScFv library, and a high affinity ScFv named MA1 was selected by phage-ELISA. Finally, after expression of MA1, we found that MA1 can specifically bind with U937 MLAA-34 positive cells, and the binding affinity of MA1 was at the nanomolar level. Furthermore, inhibition of U937 cell proliferation indicated that the novel antibody MA1 has the potential to be used as a therapeutic agent for acute monocytic leukemia.
Highlights
Acute myeloid leukemia (AML) is a common malignant disease of the blood and has rapid progression, poor prognosis, and high mortality [1]
Monocytic leukemia-associated antigen (MLAA)-34 (GenBank accession no: AY288977.2) is a novel monocytic leukemia-associated antigen that is located on chromosome 13q14.2-14.3
Our previous studies showed that MLAA-34 is an anti-apoptotic factor related closely to carcinogenesis of acute monocytic leukemia [14]
Summary
Acute myeloid leukemia (AML) is a common malignant disease of the blood and has rapid progression, poor prognosis, and high mortality [1]. Despite intensive induction therapy, where 70-80% of patients with AML achieve complete remission (CR), most patients eventually relapse and die of the disease [2]. Acute monocytic leukemia (AML-M5), as defined by the French-American-British criteria, is a distinct subtype of AML with characteristic clinical features [3]. This subtype is most frequently associated with specific chromosomal anomalies, such as t(8;16)(p11;p13), and translocation involving 11q23, including t(9;11)(p22;q23), t(10;11)(p11;q23), and t(11;19) (q23;p13) [4,5,6]. Hyperleukocytosis, extramedullary involvement, and FLT3 aberrations are associated with an unfavorable outcome in AML-M5 patients
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