Aberrant immunophenotype in acute myeloid leukemia (AML): High frequency and association with dysplasia

Abstract

17504 Background: Asynchronous expression of immunophenotypic markers on AML myeloblasts has been well described, but the association of aberrant phenotype with morphologic subclasses has not been reported previously. Methods: Multiparameter flow cytometry (MFC) data were analyzed for all patients (pts) diagnosed with AML at our institution from 2000–2006. MFC was done on fresh bone marrow aspirate and/or peripheral blood samples using the following panel of monoclonal antibodies in triple staining: CD2, CD3, CD4, CD5, CD7, CD8, CD10, CD11c, CD13, CD14, CD15, CD16, CD19, CD20, CD22, CD24, CD33, CD56, CD34, CD117, HLA-DR and TdT. Identification of myeloblasts was performed using Side Scatter (SS) characteristics and CD45 expression. Acute lymphoblastic leukemia (ALL) cases or cases with mixed lineage acute leukemia were excluded from the study. Results: We identified 76 pts with AML; median age 57, (range 10 weeks to 89 years), with 32 males and 44 females. The patients had the following French American British classification of AML: M0 (n=1), M1 (n=11), M2 (m=10), M3 (n=5), M4 (n=13), M5 (n=14), M6 (n=1), M7 (n=4) and not otherwise categorized non- M3 AML (n=17). Twenty two pts had AML with multilineage dysplasia (AML-MD) as classified by World Health Organization. Coexpression of TdT on myeloblasts was observed in 4 pts, one of these coexpressed CD5. T-cell lymphoid associated antigens (CD2, CD5 and/or CD7) were coexpressed on myeloblasts from12 pts. B cell lymphoid associated antigens (CD19 and/or CD20) were expressed on myeloblasts from11 pts. Both T and B cell lymphoid associated antigens were present on myeloblasts in 4 pts. Myeloblasts from 13 pts demonstrated the presence of the NK cell marker CD56. A total of 43 patients had AML with immunophenotypic lineage infidelity manifested by coexpression of one or more aberrant antigens on myeloblasts. The distribution of cases with lineage infidelity was higher in 22 pts with AML-MD (n=17, 77%) versus in 54 pts with no dysplasia (n=26, 48%), Chi square =5.4, p=0.02. Conclusions: Abnormal coexpression of lymphoid and NK cell markers was observed in significant number of AML pts and correlated with the presence of multilineage dysplasia. This finding may indicate an earlier stem cell origin of AML-MD. No significant financial relationships to disclose.