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Blood, 1 October 2000, Vol. 96, No. 7, pp. 2405-2411
CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS
Acute megakaryocytic leukemia: the Eastern Cooperative
Oncology Group experience
Martin S. Tallman,
Donna Neuberg,
John M. Bennett,
Christopher J. Francois,
Elisabeth Paietta,
Peter H. Wiernik,
Gordon Dewald,
Peter A. Cassileth,
Martin M. Oken, and
Jacob M. Rowe
From the Northwestern University Medical School, Robert
H. Lurie Cancer Center, Chicago IL; Biostatistics, Dana-Farber Cancer
Institute, Boston, MA; University of Rochester Medical Center,
Rochester, NY; Our Lady of Mercy Medical Center, Bronx, NY;
Cytogenetics Laboratory, Mayo Clinic, Rochester, MN; University of
Miami, Sylvester Comprehensive Cancer Center, Miami, FL; Virginia Piper
Cancer Institute, Minneapolis, MN; Rambam Medical Center, Technion
Haifa, Israel; For The Eastern Cooperative Oncology Group, Brookline,
MA.
Acute megakaryocytic leukemia (AMegL) is a rare subtype of acute
myeloid leukemia (AML) evolving from primitive megakaryoblasts. Because
of its rarity and the lack of precise diagnostic criteria in the past,
few series of adults treated with contemporary therapy have been
reported. Twenty among 1649 (1.2%) patients with newly diagnosed AML
entered on Eastern Cooperative Oncology Group (ECOG) trials between
1984 and 1997 were found to have AMegL. The median age was 42.5 years
(range 18-70). Marrow fibrosis, usually extensive, was present in the
bone marrow. Of the 8 patients who had cytogenetic studies performed,
abnormalities of chromosome 3 were the most frequent. The most
consistent immunophenotypic finding was absence of myeloperoxidase in
blast cells from 5 patients. In the most typical 3 cases, the leukemic
cells were positive for one to 2 platelet-specific antigens in addition
to lacking myeloperoxidase or an antigen consistent with a lymphoid
leukemia. Myeloid antigens other than myeloperoxidase and selected
T-cell antigens (CD7 and/or CD2) were frequently expressed. Induction
therapy included an anthracycline and cytarabine in all cases. Complete
remission (CR) was achieved in 10 of 20 patients (50%). Two patients
remain alive, one in CR at 160+ months. Resistant disease was the
cause of induction failure in all but 3 patients. The median CR
duration was 10.6 months (range 1-160+ months). The median survival for all patients was 10.4 months (range 1-160+ months). Although half of
the patients achieved CR, the long-term outcome is extremely poor,
primarily attributable to resistant disease. New therapeutic strategies
are needed.
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