Incidence, Biologic Features and Treatment Outcome of Myeloid-Antigen-Positive Acute Lymphoblastic Leukemia (My + ALL)

Detailed analyses using immunological and molecular-genetic studies have recently shown marked discrepancies between expression of lymphoid- and myeloid-associated markers in leukemic blasts compared with the majority of normal equivalent hematopoietic progenitor cells (reviewed in 11, 13, 17–19,24,45). Different hypotheses have been postulated to explain the origin of these acute leukemias with mixed-lineage features including the concept of “lineage infidelity” [42], and the theory of “lineage promiscuity” [17]. The former suggests that leukemic cells have aberrant combination of markers as a consequence of their abnormal differentiation programme and the latter assumes that these leukemias arise from the transformation of immature progenitor cells which may normally – in a transient phase of promiscuity – express characteristics of two or more cell lineages.