Background
Acute myeloid leukemia (AML) is a heterogeneous disorder characterized by clonal expansion of myeloid progenitors in the bone marrow and peripheral blood. Aspartate β-hydroxylase (ASPH) is a membrane protein that promotes cellular motion. Recent studies have revealed that ASPH is an indicator of carcinoma in humans and is highly expressed in AML.
Patients and methods
The study included 30 AML patients diagnosed and classified by complete blood count with differential, bone marrow study, flow cytometric, cytogenetic, and molecular studies, and 10 normal participants of the same age group. The serum level of ASPH was measured in both cases and controls by enzyme-linked immunosorbent assay.
Results
The level of ASPH was significantly higher in patients than in controls ( < 0.001). Patients with mutant FLT3 had higher serum ASPH compared with those with wild FLT3 with a trend toward statistical significance ( = 0.074). Other clinical and laboratory variables had no relationship with ASPH levels in the blood.
Conclusion
This study detected a significant increase in ASPH levels in the blood of AML patients more than the controls, shedding the light on the role of ASPH in AML genesis and paving the way for the development of new medications that block ASPH's leukemogenesis effect in the future.