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Year : 2016  |  Volume : 41  |  Issue : 4  |  Page : 161-167

Value of human CLEC12A expression in acute myeloid leukemia

Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt

Correspondence Address:
Gehan M Hamed
Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, 67 El Nasr Street, Sheraton Heliopolis, Cairo, 11799
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1110-1067.198648

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Background The need for identification of new specific, stable antigens during the course of acute myeloid leukemia (AML) is warranted to improve diagnosis, relapse detection, and eradication of leukemic cells. Aim We measured the surface marker human C-type lectin domain family 12, member A (CLEC12A), in 60 AML patients, 24 acute lymphoblastic leukemia (ALL) patients, and 20 controls by flow cytometry, to determine its diagnostic utility and stability in AML. Results CLEC12A was positively expressed in all studied AML patients, negative expression was detected in ALL patients, and normal CD34+ cells of the controls with significantly higher mean % expression and median fluorescence intensity was detected among AML patients (P<0.001). Receiver operating characteristic curve analysis revealed that CLEC12A at a cutoff value of at least 15.1% can diagnose and differentiate between AML and ALL with 100% sensitivity and specificity. CLEC12A was found to be positively expressed both in children and adult AML patients with significantly higher mean % expression and median fluorescence intensity in children (P=0.046), and a significant difference was found between different French–American–British Classification subtypes (P<0.001). No significant difference was detected as regards sex, newly diagnosed untreated AML patients versus AML patients in relapse (79.1±11.7 vs. 67.4±19.3, P=0.052), CD34+ versus CD34− leukemic blast cells (75.1±20.7 vs. 74.1±21.7; P=0.899), or between different cytogenetic prognostic risk groups (P>0.05). The marker was found to be positively expressed without significant difference in paired diagnosis/relapse samples, indicating its stability during the course of disease and after treatment. Conclusion CLEC12A is a specific and stable diagnostic marker of AML that could improve leukemia-associated immunophenotypes both in CD34+ and the poorly characterized CD34− patients by flow cytometry. In addition, low expression of CLEC12A on normal CD34+ progenitor cells positions the marker as a potential therapeutic target.

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