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Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, hematologic, and phenotypic features of 28 patients with acute leukemia with megakaryocytic involvement (AMKL) were analyzed. The prevalence of this type of leukemia in the entire series was 11.6%, with a higher incidence among patients with acute transformation of a previous myeloproliferative disorder (MPD) (24%) than among the transformed myelodysplastic syndrome (13%) patients. The incidence in the "de novo" ANLL was 8% and 16% among secondary leukemias. The presence of bone marrow fibrosis together with low WBC and normal or increased platelet counts despite a severe anemia are the most relevant features in these patients who otherwise displayed an apparently poor prognosis. Megakaryoblasts were morphologically recognized more frequently in the acute transformations of MPD than in de novo ANLL. Only two cases were considered pure AMKL, and in the remaining 26 patients, megakaryoblasts coexisted with other granulomonocytic and/or erythroid populations. Antiglycoprotein IIIa (anti-GPIIIa) (C17) and anti-GPIIb/IIIa (CDw41-, J15-) antibodies are probably the best markers for AMKL, although the monoclonal antibody against GPIX (FMC25) was also positive in a majority of cases but in a lower percentage of cells. On the other hand, megakaryoblasts were generally negative for granulocytic or monocytic markers (CD13, CD14, CD15); the expression of HLA-DR antigens in these cells was variable. Our present results indicate that megakaryoblastic involvement is more common than previously recognized. This is true not only in acute transformed leukemias but also in de novo ANLL. Although the diagnosis of these cases should be based on megakaryocytic markers, it is often possible to suspect a diagnosis according to certain clinical and hematologic features.
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PMID:Leukemias with megakaryoblastic involvement: clinical, hematologic, and immunologic characteristics. 316 92

Two cases of acute myeloid leukemia (FAB M1 and M2) with trisomy 4 are described. Morphologic abnormalities were confined to the granulocytic monocytic lineage with no evidence of erythroid or megakaryocytic involvement. One of the cases, who also had trisomy 13, presented initially with skin infiltration without bone marrow involvement.
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PMID:Two further cases of acute myeloid leukemia with trisomy 4. 329 70

The leukemic cells from 41 cases of acute myeloid leukemia (AML) and 17 cases of acute lymphocytic leukemia (ALL) were immunophenotyped by the alkaline phosphatase-antialkaline phosphatase (APAAP) immunocytochemical technique utilizing eight monoclonal antibodies (MoAb) reactive with cells of myeloid origin and seven MoAb reactive with lymphoid antigens. Ninety percent of the cases of AML reacted with one or more of the pan-myeloid MoAb, My7, My9, or 20.3. Reactivity of the myeloid panel of MoAb showed some correlation with the French-American-British (FAB) classification of AML. Five of six cases of acute promyelocytic leukemia (APL) were HLA-DR negative; the one HLA-DR-positive APL had a minor population of HLA-DR-negative promyelocytes. OKM5 and/or My4 reacted with 16 of 16 monocytic leukemias. No specific marker of early erythroid development was identified. AP3, a MoAb reactive with platelet glycoprotein (GPIIIa), was specific for acute megakaryoblastic leukemia. Immunocytochemistry was also helpful in classifying seven cases of AML with equivocal or negative routine cytochemistry. Two cases of AML had minor populations of blasts detected by the APAAP technique that were immunologically distinct from the major blast population; these minor populations emerged as the predominant cell type at relapse. Two cases of ALL expressed multiple myeloid and lymphoid antigens. Two other cases that morphologically were ALL reacted with only myeloid MoAb; one consisted entirely of immature basophils on ultrastructural examination. Immunophenotyping results using the APAAP technique were comparable with those obtained with flow cytometry. The APAAP technique is a reliable method for immunophenotyping leukemia that complements other methods of immunologic evaluation. The primary advantages of this method include its use with routinely prepared blood and bone marrow smears and the ability to correlate immunocytochemical reactions with morphology.
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PMID:Immunophenotyping of acute myeloid leukemia using monoclonal antibodies and the alkaline phosphatase-antialkaline phosphatase technique. 329 8

The kinetics of hematopoietic recovery after autologous bone marrow transplantation (ABMT) reflect the hematopoietic capacity of the infused marrow. In vitro treatment of marrow with high doses of mafosfamide (ASTA Z 7557) alters the hematopoietic regenerative capacity of the graft. Thirty-two patients with acute leukemia (12 acute lymphoblastic leukemia (ALL) and 20 acute non-lymphoblastic leukemia (ANLL] with 27 in complete remission and five in partial remission were consolidated with cyclophosphamide (60 mg/kg x 2) and total body irradiation (10 Gy), followed by reinfusion of autologous marrow treated in vitro with mafosfamide. The marrow of each patient had been incubated with the highest tolerable dose of mafosfamide, individually predetermined from a preincubation test. We report here that the kinetics of engraftment are strikingly different in ANLL and ALL patients. In the ANLL group recovery to 0.1% reticulocytes took a median of 20.5 days (range 14-32) versus 15 (11-28) in the ALL group; 33.5 days (18-45) versus 19 (15-30) for leukocytes to reach 1.0 x 10(9)/l; 35 (19-60) versus 20.5 (15-30) for neutrophils to reach 0.5 x 10(9)/l; 110+ (45-480+) versus 50 (23-90) for platelets to reach 50 x 10(9)/l (p less than 0.01 and p less than 0.05). Detection of granulocyte-macrophage progenitors (CFU-GM) regeneration in marrow aspirates post-ABMT was delayed in ANLL (p less than 0.05). Neither the nature of the previous induction therapy, nor the status of the blood or bone marrow at the time of collection (CFU-GM and erythroid burst-forming units/ml) nor the stem cell sensitivity to mafosfamide, nor the doses of progenitor cells infused could explain these differences. We interpreted these observations as suggesting that the engraftment potential has been more severely altered in ANLL than in ALL, which may reflect both the intensity of the in vitro treatment and the intrinsic fragility of the stem cell pool in ANLL.
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PMID:Difference in kinetics of hematopoietic reconstitution between ALL and ANLL after autologous bone marrow transplantation with marrow treated in vitro with mafosfamide (ASTA Z 7557). 333 55

We analyzed the natural history of idiopathic refractory sideroblastic anemia (IRSA) in 37 patients studied between 1969 and 1986. Although erythroid abnormalities were prominent in all, 12 patients also showed involvement of the granulocytic and/or megakaryocytic cell lines, and nonrandom chromosomal aberrations were observed in five of 23 patients studied for such defects. Measurements of erythroid marrow function showed in most cases erythroid expansion with ineffective erythropoiesis. In seven patients, however, the erythroid activity was found to be inappropriately low for the degree of anemia. Transfusion dependence occurred in 26 of 37 cases. Iron overload was a common feature at presentation but produced clinical manifestations of hemochromatosis only in those patients who subsequently had a regular need for blood transfusions. Five patients progressed to bone marrow failure, and another five patients (two of whom had monosomy 7) evolved into acute nonlymphocytic leukemia (ANLL). The median survival was 72 months, with a high transfusion requirement, multilineage defects, and inappropriately low erythroid proliferation being associated with a poor prognosis. The most common causes of death were complications of iron overload and evolution into ANLL. We conclude that (a) the natural history of IRSA is characterized by an initial phase of erythroid hyperplasia and ineffective erythropoiesis, which is usually stable for many years but in a subset of patients may be followed by a phase of marrow failure with or without the later emergence of leukemic blasts; (b) peripheral blood counts, measurement of erythroid marrow function, and chromosomal analysis are useful for identifying subjects at risk of evolution into marrow failure or ANLL; and (c) IRSA patients with no need for blood transfusions are very likely to be long survivors, whereas those who become transfusion dependent are at risk of death from the complications of secondary hemochromatosis.
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PMID:Natural history of idiopathic refractory sideroblastic anemia. 333 99

Pluripotent (CFU-MIX), erythroid (BFU-E) and granulocyte/macrophage (CFU-GM) progenitor cells were examined in bone marrow (BM) from 23 patients with myelodysplastic syndromes (MDS). Patients were grouped according to the FAB classification: Refractory anemia (RA), n = 3; RA with ring sideroblasts (RARS), n = 3; RA with excess of blasts (RAEB), n = 8; RA with excess of blasts in transformation (RAEBt), n = 7; chronic myelomonocytic leukemia (CMML), n = 2. In FAB groups RA, RARS, RAEB and RAEBt CFU-GM concentrations were normal or decreased but both CMML-patients had increased CFU-GM values. Abnormal cluster growth was observed in 9 of 23 MDS-patients. BFU-E colony formation was subnormal in all cases. Mixed-colony assay values were at the lower limit of controls in one patient and decreased in the remaining 22 MDS-patients. A similar growth pattern of hemopoietic progenitor cells was observed in 19 patients with acute nonlymphocytic leukemia (ANLL), who were studied for comparison. These data suggest a quantitative or qualitative/functional defect of the pluripotent progenitor cell compartment as the major cause for the cytopenia in MDS-patients.
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PMID:Deficiency of pluripotent hemopoietic progenitor cells in myelodysplastic syndromes. 339 Jun 17

A new reciprocal, apparently balanced translocation between chromosomes 12 and 19, t(12;19)(q13;q13.3), was detected in 5% (3/59) of patients with FAB M1 or M2 acute nonlymphocytic leukemia. In either case, this translocation was part of complex but different cytogenetic abnormalities. None of the patients had a significant response to therapy. In one instance, however, the translocation was found at first relapse after 2 years of complete remission, and no information regarding the karyotype at disease onset was available. Hematologically common to these patients were marked marrow erythroid hyperplasia and severely abnormal erythropoiesis despite normal serum B12 and folate levels. A direct association between t(12;19) and these hematologic findings will have to be established as more cases with this chromosomal abnormality are identified.
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PMID:Translocation t(12;19)(q13;q13.3). A new recurrent abnormality in acute nonlymphocytic leukemia with atypical erythropoiesis. 339 90

We have produced a monoclonal antibody (MoAb), AML-1-99, that defines a novel 124-kd protein antigen expressed on a subpopulation of monocytes and on the majority of hematopoietic progenitor cells of the granulocyte-monocyte (CFU-GM), erythroid, and mixed-lineage classes. AML-1-99 is lytic to bone marrow (BM)- and peripheral blood-derived progenitor cells in the presence of rabbit complement (C'). AML-1-99 is not toxic to progenitor cells in the absence of C', nor does it modify their growth when included in colony-forming cultures. Several leukemia cell lines, including HL-60, U937, KG-1a, and Daudi cells, express the antigen on the majority of cells. Freshly isolated leukemia cells from patients with acute myelogenous leukemia (AML) react variably with AML-1-99. Leukemia colony-forming cells from several AML patients express the antigen and could be eliminated by treatment with AML-1-99 and C'. Cell sorting and immune rosette techniques were successfully applied to normal BM and chronic myelocytic leukemia cell populations using AML-1-99 with the result that significant enrichment of CFU-GM could be accomplished. The pattern of reactivity of this MoAb and its apparent molecular weight suggests that AML-1-99 recognizes a newly defined myeloid-associated cell surface antigen.
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PMID:Distribution of the 124-kd antigen defined by monoclonal antibody AML-1-99 on normal and leukemic myeloid cells. 342 92

Marrow hematopoiesis was examined in two infants with erythroleukemia (EL) using cell culture colony assays. At diagnosis, marrow from both yielded normal to increased numbers of granulocytic colonies (CFU-C), erythroid bursts (BFU-E), and mixed colonies (CFU-GEMM), which contrasted sharply with the reduced growth in eight other newly diagnosed patients with acute leukemia. BFU-E proliferation and hemoglobinization proceeded normally in culture and was entirely erythropoietin-dependent. CFU-C colony cellular composition showed normal granulopoiesis in various stages of development. Despite low numbers of morphologically recognizable blasts in the aspirates, they were readily identified in a blast colony assay because of their high plating efficiency and high index of self-renewal on replating. Blast cells in all cultures had myeloblastic morphology, were peroxidase positive, and expressed the granulocytic-specific My-1 antigen. Monosomy 7 was seen in fresh and cultured blast cells but not in lymphocytes, indicating a clonal proliferation. After chemotherapy-induced remission, blast colonies and monosomy 7 could no longer be detected. It appears that the integrity and function of the normal hematopoietic progenitor pool were preserved in these patients with EL. The abnormal myeloblastic proliferation was expressed actively in colony assays and was useful diagnostically in these cases because marrow morphology was nondiagnostic. In these patients, EL seems to be a misnomer since the findings are suggestive of acute myeloblastic leukemia with secondary erythroid and granulocytic hyperplasia.
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PMID:Childhood erythroleukemia. Studies on pathogenesis using colony assays. 345 76

Clinical and laboratory features at presentation were correlated with morphological (FAB) subclass of AML in a group of 112 children diagnosed between 1972 and 1982. Patients with a monocytic component of AML (M4, M5) had higher initial leucocyte counts, a higher incidence of extramedullary infiltration and of CNS involvement. In M4 AML CNS relapse occurred in patients with a high initial leucocyte count whereas in M5 AML CNS involvement tended to occur at presentation in children with low initial counts. Two-thirds of patients treated achieved remission and most failures were due to inadequate chemotherapy, although haemorrhage, leucostasis or metabolic complications caused early death in patients with M4 and M5 AML. With a minimum follow up of 3 years only 12% of patients are alive; these figures have not improved in consecutive series despite increasing intensity of induction and more recent availability of bone marrow transplantation. No features predictive of long-term survival were identified, but patients with myeloid differentiation (M1, M2, M3) did better than those with a monocytic or erythroid component (M4, M5, M6). The proportion of patients with AML curable by chemotherapy seems unlikely to increase without marked intensification of post-remission chemotherapy. More aggressive CNS prophylaxis may be of benefit in cases with a monocytic component.
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PMID:Acute myeloid leukaemia in childhood: clinical features and prognosis. 346 Jun 25


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