Gene/Protein Disease Symptom Drug Enzyme Compound
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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 relationship between cell features by light microscopy and therapeutic outcome of 72 patients with acute myeloblastic leukemia (FAB M1) were investigated. The patients were divided into two groups according to myeloperoxidase-(MPO) positive percentage of blast cells, namely a low (less than 50%) and high (greater than 50%) MPO group. No remarkable morphological difference of blast cells between these two groups was observed. The 38 patients with low MPO showed a significantly lower complete response rate (CR) (52.6%) than the 34 patients with high MPO (85.3%) (p = 0.003) that included 10 CAE-positive patients and 2 ANAE-positive CAE-negative patients. The low MPO group included 5 CAE-positive patients with granulocyte dysplasia and 7 additional patients with alpha naphthyl acetate esterase (ANAE) positivity who were chloroacetate esterase (CAE) negative. Low positivity of blast cells may be due to a defective enzyme expression in the former but also may be a reflection of 'monocytic' aberrant expression in the latter. The low MPO group in M1 with this heterogeneous population is less likely to achieve CR with chemotherapy, while the high MPO group with a higher CR rate suggests a more pure entity within the myeloblastic leukemias referred to as M1. After further refinement by eliminating 24 cases that were 'esterase positive' (ANAE and/or CAE), the results were still the same, suggesting that the more immature blast populations were in the low MPO group.
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PMID:Prognostic significance of myeloperoxidase positivity of blast cells in acute myeloblastic leukemia without maturation (FAB: M1): an ECOG study. 256 Jul 75

Since myeloperoxidase (MPO) is considered to be a critical marker of differentiating acute myelogenous leukemia (AML) from acute lymphocytic leukemia (ALL), the analysis of MPO gene expression may provide further insight into the leukemia classification and the lineage fidelity of leukemia cells. By Northern blot hybridization using full-length MPO cDNA as a probe, approximately 66% of AML cells (3/4 M1 cases, 2/4 M2 cases, 15/15 M3 cases, 11/15 M4 cases, and 2/12 M5 cases) were found to express MPO mRNAs, whereas none of 18 ALL cases did. MPO mRNA was detectable when AML cells contained at least 10% peroxidase-positive cells. APL (M3) cells expressed high levels of mRNA in accordance with heavy staining for peroxidase.
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PMID:Myeloperoxidase gene expression in acute leukemias. 256 Aug 87

During the course of differentiation of early human myeloid cells toward monocytes and granulocytes, cell surface expression of the cell adhesion molecule, CD11b/CD18 (Mo1) increases dramatically and expression of myeloperoxidase (MPO), a bacteriocidal enzyme, decreases markedly. Using the inducible promyelocytic cell line HL-60 as a model, we studied the mRNA expression of these genes. Differentiation of these cells along both a monocytic and a granulocytic pathway demonstrated that the mRNA levels of the two subunits of CD11b/CD18 increased in a pattern temporally and quantitatively similar to the increase in cell surface expression of this heterodimer. In contrast, the expression of MPO mRNA decreased in a temporal and quantitative pattern similar to the known decrease in MPO protein during differentiation, suggesting that regulation of these myeloid-specific proteins may occur at the level of mRNA expression. These findings have important implications with regard to the nature of the block in differentiation in acute nonlymphocytic leukemia and the regulation of myeloid gene expression.
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PMID:Differential expression of CD11b/CD18 (Mo1) and myeloperoxidase genes during myeloid differentiation. 256 20

Mo5 is a 94-kd protein antigen expressed by human peripheral blood monocytes, neutrophils, and by all bone marrow myeloperoxidase-positive myeloid precursors (promyelocytes, myelocytes, metamyelocytes, and bands). Mo5 is borne by the malignant cells of 74% of patients (N = 27) with acute monocytic leukemia (French-American-British [FAB] group M4, M5), and 50% of patients (N = 38) with acute granulocytic leukemia (FAB M1, M2, and M3). Nonmyeloid cells in peripheral blood and bone marrow are Mo5-negative. The surface expression of Mo5 by myeloid cells is modulated by several experimental conditions: Exposure of neutrophils to calcium ionophore (1 mumol/L, 37 degrees C, ten minutes) under conditions resulting in degranulation of specific granules produces a three- to fourfold increase in the plasma membrane density of Mo5 antigen. This suggests that, in neutrophils, there is an intracellular pool of Mo5 antigen, which may be associated with specific granules, and that granule-associated Mo5 is translocated to the plasma membrane upon degranulation. Conversely, incubation of monocytes, neutrophils, U-937, and Mo5-positive leukemia cells in medium containing anti-Mo5 monoclonal antibody results in a significant decrease in surface Mo5 expression. This loss of surface Mo5 is a rapid, temperature-dependent process (occurring within 30 minutes at 37 degrees C) that is produced by divalent anti-Mo5 immunoglobulin [F(ab')2 but not F(ab)]. After down-modulation, Mo5 is reexpressed by monocytes within 48 hours. Mo5 is therefore a human myelomonocytic differentiation antigen whose expression is modulated up or down depending on the nature of extracellular stimuli.
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PMID:The modulated expression of Mo5, a human myelomonocytic plasma membrane antigen. 257 92

Cytologic and cytogenetic results obtained from patients fulfilling the FAB criteria for the diagnosis of acute nonlymphocytic leukemia (ANLL) of megakaryocytic lineage (ANLL-M7) are reported. Eleven cases were de novo ANLL-M7, of whom three presented with acute myelofibrosis. Four cases were megakaryoblastic transformations of chronic myelogenous leukemia (two cases), refractory anemia with excess of blasts (one case), and polycythemia vera (one case). Four patients showed a minority of granular blasts, with occasional Auer rods in one. Positive myeloperoxidase and/or sudan black-B stainings and CD13 positivity in these cases were consistent with the presence of a myeloid involvement. Morphologic evidence of associated myelodysplastic features was detected in all evaluable patients with de novo ANLL-M7. These cytologic findings indicate that ANLL-M7 may frequently represent a multilineage proliferation. Cytogenetic studies revealed -7/7q- and +8, alone or in combination with additional aberrations, in three cases each. Rearrangements involving bands 3q21 or 3q26 were seen in two patients and +21, as an additional aberration, in one. Other structural rearrangements all observed in a single patient were inv(16)(p13q22) at megakaryoblastic relapse with bone marrow eosinophilia, t(13;20)(q13 or 14;q11), del(20)(q11), and der(7)t(7;17)(p14;q22). Most breakpoints of these aberrations are located at bands frequently rearranged in malignant myeloid stem cell disorders. A review of 31 cases of the literature showed a frequent occurrence of -7/7q- and -5/5q- in ANLL-M7. Many of the chromosome aberrations so far described in ANLL-M7 appear to be shared by a spectrum of myeloid neoplasias and may be related to mechanisms conferring proliferative advantage to undifferentiated stem cells.
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PMID:Multipotent stem cell involvement in megakaryoblastic leukemia: cytologic and cytogenetic evidence in 15 patients. 279 Feb 2

Leukemic blasts from 40 consecutively admitted adults with untreated acute lymphoblastic leukemia (ALL) were examined for myeloid surface antigen expression. Of these, 14 (35%) were reactive with one or more myeloid monoclonal antibodies. Each example of myeloid surface antigen-positive (My+ ALL) met the standard morphologic and cytochemical criteria for ALL. In addition, none of the 13 samples studied for ultrastructural evidence of myeloperoxidase met the criteria for acute myelocytic leukemia (AML). All patient samples reacted with lymphoid monoclonal antibodies: CD10+ (8 patients), CD19+ CD10- (2 patients), T cell+ (2 patients), and T cell+ CD10+ (2 patients). Coexpression of myeloid and lymphoid determinants was established by two-color immunofluorescence studies using flow cytometry in five of five samples analyzed. Cytogenetic abnormalities that have been associated with myeloid and mixed leukemias were common, including t(9;22), 7q-, abnormalities of 11q with or without a translocation, 20q-, and -5. Blasts from seven patients were studied at the molecular level. Immunoglobulin heavy chain gene rearrangements were detected in five of five samples with B cell+ T cell- phenotypes. One sample that was T cell+ CD10+ was germline for the immunoglobulin heavy chain and the T cell receptor gamma- and beta-chain genes. The other patient with T cell+ CD10+ blasts relapsed with AML following allogeneic bone marrow transplantation. The leukemia cells at the time of diagnosis and the cells at relapse demonstrated similar cytogenetics and the same immunoglobulin gene rearrangement, suggesting a clonal relationship. As a group, the My+ ALL patients had a significantly decreased complete remission rate when compared to My- ALL patients. Further studies at the molecular level will be required to determine the significance of karyotype abnormalities in My+ ALL.
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PMID:Myeloid surface antigen-positive acute lymphoblastic leukemia (My+ ALL): immunophenotypic, ultrastructural, cytogenetic, and molecular characteristics. 281 78

A panel of eight antibodies was used by the alkaline-phosphatase/anti-alkaline phosphatase (APAAP) method to stain peripheral blood films, bone marrow smears, and cytocentrifuge preparations from 29 cases of acute myeloid leukemia. These findings were correlated with the French-American-British (FAB) classification. Leukemic cells from six cases of myeloblastic leukemia (FAB;M1) were predominantly labeled by the antimyeloperoxidase monoclonal antibody (MPO-7). Leukemic cells from the majority of eight cases of myeloblastic leukemia with maturation (FAB;M2) and progranulocytic leukemia (FAB;M3) stained with monoclonal antibodies MPO-7, NP57 (anti-elastase), and EBM11 (antimonocyte/macrophage). Leukemic cells from six cases of myelomonocytic (FAB;M4) and five cases of monocytic (FAB;M5) leukemia were most often labeled with antibodies MPO-7, NP57, and EBM11 as well as monoclonal antibodies Y1/82A (anti-monocyte) and KB90 (against the p150, 95 molecule, CD11c; a monocyte/granulocyte marker), but not with monoclonal antibody C17 (antiglycoprotein IIb/IIIa) and/or monoclonal antibody Y2/51 (antiglycoprotein IIIa). Erythroblasts from a single case of erythroleukemia (FAB;M6) were not labeled with any of the antibodies from this panel. Leukemic cells from two cases of acute megakaryocytic leukemia (FAB;M7) stained strongly with the monoclonal antiglycoprotein IIIa/IIb antibody (C17) and antiglycoprotein IIIa antibody (Y2/51). Staining by the APAAP method with this panel of antibodies was easy to perform, required no expensive instrumentation, and provided useful information in the classification of acute myeloid leukemia.
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PMID:Immunophenotyping of acute myeloid leukemia by immuno-alkaline phosphatase (APAAP) labeling with a panel of antibodies. 282 1

Since the last workshop on human leukocyte differentiation antigens, there are 14 well defined cluster-designated (CD) antigens which characterize myelomonocytic cells. Of these, 5 are potentially useful for myeloid leukemia typing (i.e. CD13, CD14, CD15, CD33, CD36) because they are cell lineage-specific and also expressed on immature cells. However, the reactivity of monoclonal anti-CD antibodies, directed against these antigens, with myeloblastic leukemia cells was found to be quite low. We produced monoclonal antibodies against myeloperoxidase. These antibodies react also with promyeloperoxidase, synthesized in HL-60 cell line cells. Monoclonal antimyeloperoxidase was found to be the most sensitive reagent to diagnose acute myeloid leukemia, even more sensitive than cytochemical stains (Sudan black, myeloperoxidase).
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PMID:Characterization of myeloid leukemia by monoclonal antibodies, with an emphasis on antibodies against myeloperoxidase. 282 87

Neutrophils and band forms from patients with acute myeloid leukemia and myelodysplastic syndrome were stained for the presence of myeloperoxidase using a cytochemical method (diaminobenzidine/hydrogen peroxide) and the alkaline phosphatase--anti-alkaline phosphatase immunocytochemical procedure (using monoclonal anti-myeloperoxidase). Neutrophils and bands were also stained for elastase and lactoferrin using monoclonal and polyclonal antibodies, respectively. Subpopulations of neutrophils and bands from cases of acute myeloid leukemia and myelodysplasia exhibited a qualitative and/or quantitative deficiency in myeloperoxidase. In addition, a quantitative decrease in elastase and/or lactoferrin staining was detected. Thus, neutrophils and bands from patients with acute myeloid leukemia and myelodysplastic syndrome have a defect in one or more of the constituents of primary and/or secondary granules. These defects are consistent with the view that abnormal neutrophils and bands are derived from a malignant clone of myeloid precursor cells.
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PMID:Abnormal neutrophils in acute myeloid leukemia and myelodysplastic syndrome. 283 2

Forty-three cases of undifferentiated leukemias by light microscopy examination were diagnosed as acute myeloblastic leukemias by ultrastructural revelation of peroxidase and were subsequently studied by immunological markers. In 41 of these cases, blasts were labeled by at least one of the antimyeloid MoAbs (My 7, My 9, and 80H5). An antimyeloperoxidase polyclonal antibody was used in 23 cases and was clearly positive in 11 of them, while cytochemistry by light microscopy was negative. These myeloblasts were frequently mixed with a minority of blasts from other lineages especially promegakaryoblasts. It is noteworthy that in 6 cases myeloid and lymphoid markers (E rosette receptor, common acute lymphoblastic leukemia antigen (cALLA), CD 9, CD 19 antigens (anti-B4 MoAb] were detected on a fraction of blast cells, suggesting a bilineage leukemia. However, in double labeling experiments, blasts with myeloperoxidase coexpressed lymphoid and myeloid markers including cALLA and CD 19 antigen. In one case, blasts had a typical non-B, non-T acute lymphoblastic leukemia phenotype (HLA-DR, CD 9, CD 19, cALLA positive) without staining by any of the antimyeloid MoAbs. However, 70% of the blasts were labeled by the antimyeloperoxidase antibody and expressed peroxidase-positive granules at ultrastructural level. In conclusion, most of the AML undiagnosed by optical cytochemistry are identified by antimyeloid antibodies. Some of these cases are also stained by some antilymphoid MoAbs. Use of antibodies against myeloperoxidase may improve the diagnosis of difficult cases of acute myeloblastic leukemia.
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PMID:Immunophenotype of leukemic blasts with small peroxidase-positive granules detected by electron microscopy. 283 65


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