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  • Title: Acute myeloid leukemias expressing lymphoid-associated antigens: diagnostic incidence and prognostic significance.
    Author: Drexler HG, Thiel E, Ludwig WD.
    Journal: Leukemia; 1993 Apr; 7(4):489-98. PubMed ID: 7681917.
    Abstract:
    A portion of patients with acute myeloid leukemia also display surface antigens associated with lymphoid development (Ly+AML). The incidence of Ly+AML varies considerably between independent studies, both overall and with regard to individual antigens. On average, lymphoid-associated antigen expression is relatively low in AML. The reasons for some striking differences between conflicting reports are not clear, but are most probably due to various technical aspects including several arbitrary parameters. The data accumulated from the literature lead to the following conclusions: (i) use of different reagents against the CD surface antigens, different positive/negative cut-off levels, analysis of fresh or frozen cell material and variable sensitivities of the analytical instruments (expression of lymphoid-associated antigens was commonly weaker than myeloid-associated markers) seriously influence the results; (ii) most antigens (CD1, CD2, CD3, CD5, CD8, CD10, CD19, CD20, CD21, CD22) were expressed on less than 10% of AML cases; (iii) the CD4 and CD7 antigens, also found on normal monocytic and immature myeloid progenitor cells, were detected in 24% and 15% of AML cases, and their expression correlated with FAB M4/M5 and M1/M2 morphology, respectively; (iv) differences between pediatric and adult Ly+AML were restricted to CD4 and CD19 expression being detected more often in childhood cases; (v) there is no cytogenetic anomaly specific for Ly+AML; anomalies exclusively associated with lymphoid malignancies were not seen; aberrations involving 11q23, 14q32, and the 9;22 translocation seem to be increased; (vi) in most studies, expression of lymphoid-associated antigens (with the exception of CD7) on AML blasts lacked prognostic significance; CD7+AML appears to be a particular subset of malignant myeloid progenitors. In summary, these findings suggest that in general, Ly+AML may not represent a biologically distinct form of leukemia as these cases have similar clinical features and respond to therapy in a comparable manner.
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