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)

A monoclonal antibody, NP57, was produced and used against the neutrophil granule protein elastase, which selectively stain neutrophils in cryostat and paraffin wax sections. The antibody stains neutrophils and a subpopulation of monocytes in blood smears and neutrophil precursors in bone marrow smears, and gives positive reactions with the cell lines HL60 and U-937. It labelled the blast cells in 68% of cases of acute myeloid leukaemia (M1-M5) but was unreactive with all cases of lymphoid leukaemias. Most of the elastase negative myeloid leukaemias were labelled by monoclonal anti-myeloperoxidase (antibody MPO-7) as were cells from the promyelocytic line HL60. No cases of myeloid leukaemia showed the opposite pattern--that is elastase positive, myeloperoxidase negative, suggesting that the production of myeloperoxidase precedes the onset of elastase synthesis during myeloid maturation. The anti-elastase antibody NP57 is a useful addition to the range of monoclonal antibodies available for the differential diagnosis of acute leukaemia by alkaline phosphatase-antialkaline phosphatase (APAAP) labelling of cell smears; it may also be of value for the histopathological diagnosis of tumour deposits in myeloid leukaemia and for the detection of neutrophils in paraffin sections.
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PMID:Use of monoclonal antibody against human neutrophil elastase in normal and leukaemic myeloid cells. 284 60

This thesis is a survey of nine previously published articles on MPO deficient PMN. The incidences in leukaemia and allied disorders of the presence of this abnormal subpopulation of mature neutrophils and the relationship to clinical course in AML, susceptibility to infections in AML, FAB classification in AML and MDS, cytogenetically defined aberrations in MDS and morphometrical characteristics were investigated. The aims of the studies were to examine the diagnostic as well as the prognostic value of the parameter, to examine the usefulness of the parameter as an predictive indicator of CR and relapse in AML and to examine the concept that MPO deficient PMN may originate from leukaemic precursors. MPO deficient PMN were found to occur in a minor number (less than 4% of the total number of PMN) in normal humans and the incidences of an abnormal number (greater than 4%) were found to be about 40% in AML (I, II, III, IV, VIII), 60% in CML (I, VII), 30% in MPD other than CML (VII) and 30% in MDS (V). The highest incidences in AML were found in the FAB subtypes possessing the most myeloid differentiation potential i.e. FAB M2 and FAB M4 (IV). In ALL, CLL, HCL, Hodgkin's disease, anaemia not related to leukaemia and leukaemoid reactions the incidences all were 0% (I, unpublished data). The abnormal MPO deficient PMN subpopulation, if present, disappeared when CR was achieved and reappeared when relapse eventually was developed (II, VIII). In both situations serial determinations showed that the change occurred before the usual routine blood examinations predicted CR and relapse; several days and several months prior, respectively (VIII). The probability of obtaining CR was lower in the AML patients with the abnormal subpopulation and the risk of developing relapse higher than in AML patients without the anomaly (II, VIII). These differences were not statistically significant, however. AML patients, showing an increased number of MPO deficient PMN, revealed a statistically significant increased susceptibility to infections (P less than 0.01) during the preremission phase accounting for 18% to 67% of the total number of infections in this period (III). This increase was positively correlated to the extent of the anomaly (P less than 0.002). The spontaneous occurrence of a subpopulation of MPO deficient PMN in MDS went together with a simultaneous progression in cytogenetically determined clonal chromosomal aberrations and were related to progression in FAB subtype as well (VI). Morphometrically MPO deficient PMN were characterized by a decreased total cell size and an increased nucleus size of the projected images (IX).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myeloperoxidase deficient polymorphonuclear leucocytes in leukaemia and allied disorders. 285 15

Quantitative estimations of the mean areas of cell, nucleus and cytoplasm in polymorphonuclear leucocytes (PMN) were performed by automated image analysis of blood smears from six patients with acute myeloid leukaemia. The PMN were qualitatively separated by a cytochemical staining method into two well-defined subpopulations i.e. myeloperoxidase (MPO)-normal and MPO-deficient PMN. MPO-deficient PMN were characterized by a decreased size of the total cell (P less than 0.01), an increased size of the nucleus (P less than 0.01) and a decreased size of the cytoplasm (P less than 0.01). The resulting highly increased nucleus-to-cytoplasm ratio in this specific PMN subpopulation bears a striking resemblance to cells in malignant tumours. The planimetric results in this study further support the concept that MPO-deficient PMN may be the progeny of leukaemic precursors.
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PMID:Myeloperoxidase deficient polymorphonuclear leucocytes: computerized planimetric estimations of cellular and nuclear size. 288 56

In 148 consecutive cases of untreated acute myeloid leukaemia (AML) the relation between an increased number of myeloperoxidase (MPO)-deficient polymorphonuclear leucocytes (PMN) and a classification modified after the proposals outlined by the French-American-British Co-operative Group, the FAB classification, was investigated. In 22 cases with minimal granulocytic component, 8 M5, 13 M6, 1 M7, no one (0%) showed an increased number of MPO-deficient PMN. In 3 (13%) of 23 cases with slight granulocytic component, 3 M0, 20 M1, and in 49 (57%) of 86 cases with granulocytic differentiation (53 M2, 1 M3, 32 M4), an increased number was demonstrated. This difference was statistically significant at a high level (P less than 0.0001). The number of MPO-deficient PMN could not be estimated in 15 cases of AML and 2 additional cases were mixed leukaemias. It is concluded that an increased number of MPO-deficient PMN in acute leukaemia speaks in favour not only of AML, but suggests the diagnosis of subtypes with some granulocytic component, most likely M1, M2, M3 or M4. Furthermore, the results support the concept that in AML at least some of the mature myeloid cells may be involved in the leukaemic process.
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PMID:Myeloperoxidase-deficient polymorphonuclear leucocytes. (IV): Relation to FAB-classification in acute myeloid leukaemia. 299 22

In 45 cases of primary myelodysplastic syndrome; 16 refractory anaemia (RA), 11 RA with ring sideroblasts (RA+), 13 RA with excess of blasts (RAEB), 5 chronic myelomonocytic leukaemia (CMML), the relations between myeloperoxidase (MPO) activity in polymorphonuclear leucocytes (PMN), neutrophil alkaline phosphatase (NAP) activity, absolute number of PMN and thrombocytopenia were investigated. 11 patients (26%) showed abnormal numbers (greater than 4%) of MPO-deficient PMN and 27 (75%) showed abnormal NAP activity (NAP score; greater than 134.0, less than 15.0), mostly decreased. No significant correlations between MPO activity and NAP activity were demonstrated, nor were any significant correlations found with the other parameters investigated. The FAB-subtypes, RAEB and CMML, showed a significant correlation to thrombocytopenia (p = 0.028) and to pancytopenia (p = 0.024). The findings may support the view that at least some of the myelodysplastic syndromes may be fundamentally the same disease as acute myeloid leukaemia.
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PMID:Myeloperoxidase-deficient polymorphonuclear leucocytes. (V): Relation to FAB-classification and neutrophil alkaline phosphatase activity in primary myelodysplastic syndromes. 299 23

A study was made of in vitro antibody-dependent cellular cytotoxicity of neutrophils of peripheral blood in 14 cases of acute myeloblastic leukemia and in 20 healthy patients (control group). A decrease in the number of neutrophils, carrying receptors to Fc-IgG and to C3b-component of complement was registered compared to the results obtained for healthy people. Besides, the number of cells restoring Nitro-blue tetrazolium and myeloperoxidase activity decreased. The decrease in antibody-dependent cellular cytotoxicity of neutrophils in the cases of acute myeloblastic leukaemia is explained by the deficiency of the cell receptor apparatus and by the decrease in the intracellular metabolism in them.
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PMID:[Antibody-dependent cell-mediated cytotoxicity of peripheral blood neutrophils in vitro in acute leukemia]. 299 55

We report a case of a 71-year-old female patient with an unusual morphological variant of Philadelphia chromosome-positive, acute nonlymphocytic leukemia. The myeloblasts exhibited an extreme degree of lipid vacuolization and the serum exhibited hyperlipidemia. The initial serum triglyceride level was 756 mg/dL. There were 26,000 white blood cells per cubic millimeter with 19% myeloblasts. The bone marrow contained greater than 80% myeloblasts that were myeloperoxidase- and chloracetate esterase-positive and typed positive for OKM1 and Leu 1 myeloid cellular markers. At remission, the lipid inclusions disappeared and the serum triglyceride levels returned to normal. Both abnormalities recurred at relapse. The cause of the hyperlipidemia and lipid inclusions was most likely an acquired hyperlipoproteinemia and secondary absorption of lipids into the malignant cells.
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PMID:Hypertriglyceridemia and lipid inclusions in a case of Philadelphia chromosome-positive, acute nonlymphocytic leukemia. 300 73

In 98 patients with chronic myeloproliferative disorders (45 chr. myeloid leukaemia (CML), 19 myelofibrosis primaria (MP), 28 polycythaemia vera (PV) and 6 idiopathic thrombocythaemia (IT)) the incidences of increased numbers of MPO-deficient polymorphonuclear (PMN) were 60% in CML, 32% in MP, 7% in PV and 0% in IT patients. The CML figure differed significantly from the others (p less than 0.001). This study confirms the finding of low NAP scores in CML compared to normal or high NAP scores in the other groups of the myeloproliferative syndrome. The incidences of increased numbers of MPO-deficient PMN in this study are comparable to those found in the primary myelodysplastic syndromes and in acute myeloid leukaemia. The finding supports the view that some of the CML cases and may be other cases of the chronic myeloproliferative disorders may be fundamentally the same disease as in primary myelodysplastic syndromes and in acute myeloid leukaemias.
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PMID:Myeloperoxidase-deficient polymorphonuclear leucocytes (VII): Incidence in untreated myeloproliferative disorders. 300 24

Serial determinations of MPO and NAP activities in granulocytes were performed during the preremission phase and the remission phase in patients with AML. Of 18 patients examined during the preremission period, 9 showed an increased number of MPO deficient PMN. Complete remission was attained in 4 of these, in 3 the number of abnormal granulocytes changed to normal 7, 7 and 14 days before and in 1 simultaneously with the attainment of complete remission. In the other patients no changes in granulocyte MPO activity occurred during the preremission period. All 20 patients examined during complete remission showed a normal MPO activity in granulocytes. Of eight patients, who at diagnosis had shown abnormal granulocyte MPO activity, three developed relapse. In two of these, an increased number of MPO deficient PMN reappeared two and eight months prior to and in one simultaneous with clinical and laboratory suspicion of relapse. A statistically significant relation between low NAP scores and an increased number of MPO deficient PMN was found (P = 0.011). Serial determinations of MPO activities in PMN, although restricted to cases of AML with initially abnormal values, may prove helpful in predicting achievement of complete remission and may furthermore prove to be useful as an indicator of early relapse.
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PMID:Myeloperoxidase-deficient polymorphonuclear leucocytes. Longitudinal study during the preremission--and the remission phase in acute myeloid leukaemia. Comparison to neutrophil alkaline phosphatase (NAP) activity. 300 94

The techniques of transmission electron microscopy (TEM), including ultrastructural myeloperoxidase cytochemistry (MPO), and immunological marker analysis, have been used to classify 58 "difficult" cases of acute leukemia where a precise diagnosis could not be made on the basis of conventional light microscopy and cytochemistry. TEM with MPO proved most valuable in characterizing 15 cases of acute myeloid leukemia and its variants, as well as defining complex cellular subpopulations in 11 cases of chronic myeloid leukemia in blast crisis. Immunological marker studies provided conclusive evidence of lymphoid differentiation in 18 cases of acute lymphoblastic leukemia and related disorders. In addition, the combined techniques were used to document 14 cases of terminal transferase-positive acute myeloid leukemia. This study demonstrates that these 2 techniques provide overlapping and complementary information for accurate diagnosis and classification of morphologically difficult hematological malignancies.
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PMID:Characterizing "difficult" acute leukemias. A combined electron microscopic and immunological marker study. 301 25


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