Phenotype of early erythroblastic leukemias

Abstract

Nine cases of early erythroblastic leukemia, unidentified by usual criteria, have been diagnosed using a panel of antibodies. Three cases arose in patients with Down's syndrome, one in a patient with therapy- related leukemia, and four patients were in blast crisis of chronic myeloid leukemia; only one case arose de novo. Blast cells could be assigned to two main stages of erythroid differentiation: presence of all erythroid-specific proteins in two patients, a phenotype corresponding to an immature erythroblast; absence of the erythroid markers such as glycophorin A and spectrin in the presence of carbonic anhydrase isoenzyme I, ABH group antigens, and the antigen defined by FA6 152 monoclonal antibody in six patients, a phenotype related to a late erythroid progenitor (CFU-E). One patient had an intermediate phenotype. All patients except one demonstrated a megakaryocytic component. In three patients, chromosomal abnormalities were present, detected both in blasts and in erythroid colonies. In conclusion, these findings indicate that most “cryptic erythroleukemias” are blocked at a “CFU-E-like” stage of differentiation, it may be a frequent event in Down's syndrome and chronic myeloid leukemia, and these erythroleukemias are phenotypically heterogeneous.

Expression of erythroid‐specific genes in acute megakaryoblastic leukaemia and transient myeloproliferative disorder in Down's syndrome

“…The overlap of M6 and M7 cell phenotypes seems to be the reflection of close relationship between erythroid and megakaryocytic lineages. Since most of M7 blasts expressed erythroid specific genes, it is very difficult to distinguish M7 from erythroleukaemia especially in which leukaemic cells are blocked at an early stage of erythroid differentiation (Villeval et al, 1986). M6 and M7 leukaemias are quite heterogenous at the cellular level and arise from blockages at different stages of erythroidmegakaryocytic differentiation.…”

Autocrine stimulation by erythropoietin and autonomous growth of human erythroid leukemic cells in vitro.

“…1, 2, 4, 5, 6, 1 1, and 12) (16). The diagnosis ofearly erythroid leukemia was ascertained when differentiation markers showed the presence of CAl and CD36 and, occasionally, GPA on blast cells and ferritin aggregates and 0 granules were revealed by ultrastructural studies (3,9). The percentage of blast cells was > 90% after Ficoll-metrizoate gradient separation of blood or marrow samples.…”

“…Recently, we and others (3-7) have identified a new type of erythroleukemia in which leukemic cells are blocked at an early stage of erythroid differentiation and are not morphologically identifiable. In the absence ofdifferentiation markers, these forms are classified as either undifferentiated, lymphoblastic, or even monoblastic leukemias and have been termed cryptic erythroleukemia (4) or early erythroid leukemia (3).…”

“…These early erythroid leukemias can be subclassified into two types (3). One corresponds to cells blocked at a stage of differentiation identical to that of CFU-erythroid.…”

“…The main differentiation markers expressed are carbonic anhydrase 1 (CAl1)', cluster ofdifferentiation 36 (CD36), glycophorin C (3), transferrin receptors, and often A, B, and H blood groups. In the second, the erythroid leukemic cells correspond to proerythroblasts or pre-proerythroblasts (8), with the presence of glycophorin A (GPA) but rarely of hemoglobin (3). These erythroid leukemic cells have specific ultrastructural characteristics which include the presence of ferritin aggregates and peculiar 0 granules (7,9).…”