Clinical, morphologic, and cytogenetic characteristics of 26 patients with acute erythroblastic leukemia

Abstract

We have performed a retrospective analysis of the clinical, morphologic, and cytogenetic findings in 26 patients diagnosed between January 1969 and September 1991 with acute erythroblastic leukemia de novo (EL or AML-M6). Clonal chromosomal abnormalities were found in 20 (77%) patients (95% confidence interval [CI], 61% to 93%). Loss of all or part of the long arm (q) of chromosomes 5 and/or 7 was observed in 17 (65%) patients (95% CI, 47% to 83%). In addition, the karyotypes were often complex, with multiple abnormalities and subclones. Among the remaining nine patients, six had a normal karyotype and one each had trisomy 8, t(3;3), or t(3;5). The overall frequency of abnormalities of chromosomes 5 and/or 7 observed in our M6 patients is similar to that observed in our patients with therapy-related acute myeloid leukemia (t-AML; 99 of 129 patients, 77%), but substantially higher than that noted in our other patients with AML de novo (French- American-British [FAB] subtypes M1-M5: 52 of 334 patients, 16%). Our M6 patients with abnormalities of chromosomes 5 and/or 7 were older and had a shorter median survival (16 v 77 weeks [P = .005]) than did the M6 patients without these abnormalities. We found no correlation between morphologic features and either cytogenetic abnormalities or clinical outcome. Of note was the finding that the percentage of myeloblasts, which may account for only a small fraction of the total marrow elements when the revised FAB criteria are applied, had no bearing on prognosis. We conclude that acute erythroblastic leukemia, when defined by morphologic criteria, consists of two distinctive subgroups: one group tends to be older, has complex cytogenetic abnormalities, especially of chromosomes 5 and/or 7, and shares biologic and clinical features with t-AML; the other group, with simple or no detectable cytogenetic abnormalities, has a more favorable prognosis when treated with intensive chemotherapy.

Acute myeloid leukaemia (M6B: pure acute erythroid leukaemia) in a Thoroughbred foal

“…8,10 Acute erythroid leukaemias (subtypes M6A and M6B) are aggressive neoplasms, associated with a poor prognosis, poor response to chemotherapy and a median survival time of 3.5 months in humans. 28,[33][34][35] In summary, this case report describes a myeloproliferative disease in a 10-week-old filly that was identified after bone marrow evaluation as acute erythroid leukaemia. The absence of abnormal circulating neoplastic cells highlights the importance of considering both haematological and bone marrow cytological findings to establish a diagnosis of AML M6B (pure acute erythroid leukaemia).…”

dic(5;17): A recurring abnormality in malignant myeloid disorders associated with mutations ofTP53

“…However, the frequency of these abnormalities differs among the various FAB subgroups. Whereas only 6.3% (67/ 1060) of patients who had AML M1-M5 de novo had complete or partial monosomy for 17p, 31% (15/48) of AML-M6 patients had this abnormality (Olopade et al, 1992). In t-MDS/t-AML, 15% (37/246) of patients had loss of 17p.…”

Transcriptional regulation of erythropoiesis

“…EKLF expression is remarkably restricted to erythroid, megakaryocytic and mast cells [55]. The human EKLF gene was located to chromosome 19p13, a region deleted in some cases of human erythroleukemia [56].…”