Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

A fluorometric enzyme immunoassay using an alkaline phosphatase-conjugated monoclonal antibody was developed to quantitate feline leukemia virus (FeLV) infection. Monoclonal antibodies, directed against the FeLV structural protein p27, were conjugated with alkaline phosphatase using a modified maleimide method. The enzyme immunoassay requires only 4 days to reproducibly measure FeLV production instead of the 12 days required for the commonly used transformation assay using C81 cells. A linear correlation was found between the virion associated reverse transcriptase activity and the amount of intracellular p27 as determined by the fluorometric enzyme immunoassay. An immunocytochemical assay using the same conjugated monoclonal with a different substrate gave visible plaques in infected cell monolayers and was therefore used to titrate FeLV in plaque-forming units. The results obtained by all the procedures followed single hit kinetics for FeLV infection. The fluorometric enzyme immunoassay was adapted to measure FeLV neutralizing antibodies, allowing a sensitive and accurate determination of neutralizing titers.
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PMID:Fluorometric enzyme immunoassay for measurement of infectious feline leukemia virus and its neutralization. 284

A case of complete remission of adult T-cell leukemia (ATL) induced by beta-interferon is reported. A 46-year-old male was diagnosed as ATL because of the increased number of ATL cells with deeply indented and lobulated nuclei in the peripheral blood, accompanied by elevated values of the lactic dehydrogenase, the alkaline phosphatase, and the calcium in the serum. The result of the cell surface marker analysis of peripheral blood lymphocytes was compatible with ATL and anti-ATL associated antibody (ATLA) was positive. The integration of proviral deoxyribonucleic acid (DNA) of human T-cell leukemia virus type I(HTLV-I) was proved in the peripheral blood lymphocytes using Southern blot hybridization. Since an ordinal chemotherapy was not so effective for this patient, he was treated with 1.8 X 10(7) units of recombinant beta-interferon (beta-IFN) per day for 7 days as one course. After 5 courses of treatment, a markedly favorable response was recognized, and he achieved complete remission. A lower dose of beta-IFN (9 X 10(6) units per day for 3 days as one course, one or two courses per month) has been continued and he has still been in a complete remission state for 10 months. It is concluded that beta-IFN should be used to treat ATL.
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PMID:A first case of complete remission of beta-interferon sensitive adult T-cell leukemia. 289 May 36

The phospholipase A2 inhibitory activity of a 38 kDa K+-sensitive actin gelation factor in a murine leukemia cell line (M1) was examined. A specific antibody against 38 kDa protein was found to cross-react with 37 kDa protein (lipocortin) in rat peritoneal exudates. Although the native 38 kDa protein from M1 cells did not block phospholipase A2 activity, pretreatment with alkaline phosphatase produced a form that did inhibit this enzyme. However, a purified 38 kDa protein from differentiated M1 cells blocked phospholipase A2 activity without pretreatment with alkaline phosphatase. Phospholipase A2 inhibitory activity of the 38 kDa protein was not altered by addition of actin. These findings suggest that the phospholipase A2 inhibitory of our 38 kDa protein was induced during differentiation. We also proposed that our 38 kDa protein has the same epitope as lipocortin.
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PMID:Changes of phospholipase A2 inhibitory activity in the K+-sensitive actin gelation factor during the differentiation of myeloid leukemia cells. 295 92

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

The risk of development of CNS leukemia was investigated in 153 adults with acute lymphocytic leukemia (ALL) who received systemic combination chemotherapy without CNS prophylaxis. Overall, 31 patients (20%) developed CNS leukemia after a median of 6 months of therapy; the estimated 1-year incidence of CNS leukemia was 21% (SE, 3.9%). Characteristics significantly associated with CNS involvement included the presence of elevated hemoglobin creatinine, alkaline phosphatase, fibrinogen, and lactic dehydrogenase levels; B-cell leukemia; and high leukemic cell proliferative activity. Multivariate analysis identified lactic dehydrogenase levels of greater than or equal to 600 U/L and greater than or equal to 14% of cells in the S + G2M compartment to have independent additive poor prognostic significance. Patients were categorized into different risk groups for CNS leukemia with 1-year incidences ranging from 4% to 55%. While related to a high occurrence of CNS leukemia at diagnosis (33%) and subsequently (100%), the low incidence of B-cell disease excluded it from the multivariate analysis. The use of systemic chemotherapy containing multiple agents with good CNS penetration and in high doses (VAD regimen) in 90 patients was associated with a trend for lower CNS leukemia at 1 year (15% v 31%), especially in the low-risk category. We propose to develop future therapies for adults with ALL that include risk-oriented CNS prophylactic approaches.
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PMID:Identification of risk groups for development of central nervous system leukemia in adults with acute lymphocytic leukemia. 305 30

Sixty-nine patients with hairy-cell leukemia (HCL) were treated with interferon alfa-2b (IFN) in a single-institution study. The dose used was 2 x 10(6) U/m2 self-administered subcutaneously three times weekly, for a planned treatment duration of 12 to 18 months. Of the 68 evaluable patients, the major response rate was 75%, with 13% complete responses (CRs) and 62% partial responses (PRs). An additional eleven patients (16%) had minor responses (MRs). Duration of response was denoted as failure-free survival (FFS), defined as the time from the end of IFN therapy to a need for further antileukemic therapy. Of the 60 responding patients followed after discontinuation of IFN, 27 have relapsed, requiring further therapy. The median actuarial FFS for these 60 patients is 25.4 months. All but five patients are alive, and the actuarial overall survival for the 69 patients is 91% +/- 4% at 4 years from the start of IFN. The best indicators of relapse were the neutrophil alkaline phosphatase (NAP) score and degree of residual bone marrow hairy cells (%HCL) at the completion of therapy. Patients with NAP less than 30 (n = 21) had the best prognosis (median FFS, 30.4 months), while those with NAP greater than or equal to 30 and %HCL less than or equal to 30 (n = 21) or %HCL greater than 30 (n = 16) had intermediate and poor prognoses, respectively (median FFS, 23.5 and 12.4 months) (P = .0005). Fourteen of the relapsing patients are evaluable for response to a second course of IFN, with seven PRs and four MRs. Stratified randomized trials are indicated to determine the role of maintenance therapy for responding patients.
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PMID:Relapse after interferon alfa-2b therapy for hairy-cell leukemia: analysis of prognostic variables. 305 3

Studies of bone cells in culture have raised two salient questions: are the findings representative of the in vivo situation and can the conflicting data from different cell models be reconciled? Review of the literature indicates that all osteoblastic cells, defined by their origin or by their ability to produce mineralized matrix, have a few common properties: production of type I collagen; increased alkaline phosphatase activity; and parathyroid hormone-stimulated adenylate cyclase. Other features, such as osteocalcin and prostaglandin E production and the response to prostaglandin E, are selectively expressed by certain cell types. Pilot studies on mRNA levels of 'bone proteins' in developing calvaria suggest that such differences may reflect stages in osteoblastic differentiation. Immortalization of calvaria-derived cells using a SV40 large T antigen vector, which may freeze the cells in their particular state of differentiation (as proposed for leukaemia cells), yields phenotypes consistent with that hypothesis. Immortal cell lines may thus help to characterize osteoblastic differentiation. The diversity of osteoblast responses in culture to hormones and growth factors could be due to these phenotype differences but could also represent a subspecialization of differentiated cells. In addition, in the organism regulatory agents act in concert on a heterogeneous interactive cell population. Nonetheless cell cultures can be useful in screening for and predicting in vivo responses, as was shown by the 1,25-(OH)2D3 stimulation of osteocalcin, and for studying the molecular mechanisms of regulatory effects. Cell lines are also convenient for the production of specific proteins and cDNA libraries, and for the expression of specific genes.
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PMID:Diversity of the osteoblastic phenotype. 306 18

Using a panel of monoclonal antibodies for the immunophenotyping of haematological malignancies, we have made a direct comparison of the usefulness of indirect immunofluorescence using flow cytometry (IFC) alongside the alkaline phosphatase-anti-alkaline phosphatase (APAAP) immunoenzyme method. Analysis of 400 consecutive patient samples (blood and bone marrow) over a 2-year period, resulted in unequivocal phenotyping agreement by both methods in 98 per cent of cases. The positive results accounting for 2 per cent discordance were obtained by the APAAP method. The value of the technique in the clinical management of patients with leukaemia is documented together with guidelines for clinical laboratories.
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PMID:Immunophenotyping of leukaemias by flow cytometry and APAAP: a two-year comparative analysis in hospital practice. 306 83


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