Lineage infidelity in acute leukemia

Abstract

Blast cells from 20 patients with acute leukemia (13 diagnosed myeloblastic and 7 as lymphoblastic, using the FAB classification) were studied using antibodies to lineage-specific differentiation markers. The phenotypic findings were usually consistent with the clinical diagnosis. However, examples were encountered where individual blast cells had a cytoplasmic marker of one lineage and a surface marker of a different lineage (lineage infidelity). Six examples of intramyeloid (two different myeloid lineages in the same cell) and three examples of interlineage infidelity (myeloid and lymphoid markers in the same blast cell) were encountered. No doubly marked cells were found in control material consisting of normal marrow cells, marrow regenerating after transplantation, or multilineage colonies derived from marrow in culture. A significant trend was observed relating the presence of lineage infidelity and failure of remission-induction. The data are interpreted as support for abnormal gene expression in leukemia.

Changes in self‐renewal potential of human leukemic cells (K562): A bidirectional stochastic process

“…It has been suggested that during this predeterministic stage, normal pluripotent stem cells might express all of the lineage markers that characterize their differentiated progeny and that restriction to a single lineage is seen only postdetermination (Till, 1976). In line with this, the recently described simultaneous presence of multilineage markers on the surface of various leukemic cells including K562 (Fioritoni et al, 1980;Marie et al, 1981;Smith et al, 1983) may in fact indicate that the differentiation program of these cells is blocked a t a predeterministic stage.…”

Chemotherapy of myeloma: Drug combinations versus single agents, an overview, and comments on acute leukemia in myeloma

“…The peripheral blood cells were tested with 2 I different monoclonal antibodies designed to react with markers specific for granulocytic (Myl), monocytic, erythroid, megakaryocytic, T-cell and B-cell features. (The methods and the panel of monoclonal antibodies employed are describedin Smith et al, 1983). We found that…”

Flow cytometric determination of atypical antigen expression in acute leukemia for the study of minimal residual disease

“…The approach to distinguish between leukemic and normal bone marrow cells is based on the fact that leukemic cells do not necessarily exhibit antigenic features that are characteristic of their nonmalignant counterparts (14,15). Specifically, antigen combinations were regarded as leukemia associated by the following criteria: coexpression of antigens that are found on different lineages in normal hematopoietic cells, i.e., lymphoid and myeloid restricted antigens (8,17,22,25); unphysiological coexpression of immature and mature antigens within a certain differentiation lineage (CD34 and CD15 in AML, CD34 and CD22 in ALL) (15,19,27,28); lack of a n antigen that should be present during normal differentiation (lack of CD33 or CD13 on myeloblasts, lack of Leu-M3 expression on MY-4 positive monocytes, HLA-DR negative myeloblastsimonocytes) (24,(27)(28)(29); and immunophenotypes that are absent or exceedingly rare in normal bone marrow (coexpression of TdT and early T-cell antigens, e.g., CD5, coexpression of TdT, and CD33iCD13) (1,131.…”