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 complete lack of myeloperoxidase (MPO) was demonstrated in a boy suffering from acute myeloic leukemia during the acute phase of the disease and after a remission was achieved. A partial defect of MPO was demonstrated in the patient's father, no further abnormalities were seen in other members of the family. The fine structure of the patient's neutrophils and monocytes appeared normal, no activity of MPO was demonstrated on the fine structural level. In the father's neutrophils transitional forms between cells exhibiting a normal MPO activity and those without activity were demonstrated. The neutrophil bactericidal activity was strongly inhibited in the patient and decreased in his father. Normal values were found in: NBT test, chemotaxis, serum-dependent phagocytosis, number of B and T lymphocytes, serum immunoglobulins, and complement. A possible connection between MPO deficiency and leukemia is discussed.
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PMID:[Familial peroxidase-deficiency and acute myeloic leukemia (author's transl)]. 20 71

A patient with acute leukemia and an IgM, kappa (IgMkappa) monoclonal gammopathy, Bence-Jones proteinuria, and blasts containing intracytoplasmic vacuoles with peroxidase-positive inclusions is discussed. Special stains, immunofluorescence, and electron microscopy suggested that the vacuoles were autophagosomes containing Auer-body-like inclusions, and that the blast cells did not synthesize the paraprotein. Chemotherapy with cyclophosphamide, vincristine, and prednisone resulted in transient improvement of the leukemia, but the level of the paraprotein was unchanged. Other case reports involving monoclonal gammopathy in association with acute leukemia are reviewed and contrasted with this case.
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PMID:Blast cell leukemia with IgM monoclonal gammopathy and intracytoplasmic vacuoles and Auer-body-like inclusions. 21 43

Enzymatically homogeneous populations of lymphocytes, monocytes, and neutrophils were isolated by zonal centrifugation from 5 untreated patients with chronic lymphocytic leukemia (CLL) and 2 patients with CLL in full remission. The cells were then quantitatively analyzed for six leukocytic enzymes and compared with cells from normal subjects. CLL monocytes were deficient in beta-glucuronidase (0.06 units; normal, 0.16), myeloperoxidase (0.07 mg; normal, 0.5 mg), and lysozyme (0.7 mg; normal, 3.3 mg). In 2 cases, CLL neutrophils were severely deficient in lysozyme (1 to 2 mg; normal, 7 mg) and myeloperoxidase (2 to 3 mg; normal, 7 mg). Neutrophil alkaline phosphatase and neutral protease were unaffected. CLL lymphocytes shared with the monocytes the deficiency of beta-glucuronidase (0.03 units; normal, 0.09 units). The 2 CLL patients in full remission carried normal enzyme levels in leukocytes of all three cell lines. The CLL lymphocytes of untreated patients were unresponsive to mitogens but became responsive in remission. The CLL monocytes from both untreated and treated patients transformed into macrophages. The pattern of shared enzyme deficiency among lymphocytes, monocytes, and neutrophils of CLL patients and its normalization in all three cell types under remission suggest that the differentiation of the three leukocytic cell lines may be an enzymatically interlinked process and that the deficiency of these enzymes in leukemia may reflect an interrelated aberrant differentiation of the leukemic cells.
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PMID:Monocyte and granulocyte defect in chronic lymphocytic leukemia. 21 99

Line 1, a spontaneous alveolar carcinoma from a BALB/c mouse, is highly metastatic and weakly antigenic in the syngeneic host. Sera and enriched antibody preparations were made specific for line 1 cells by in vitro and in vivo absorptions. By lactoperoxidase-catalyzed radioiodination of cell surface protein followed by precipitation with specific antibodies, a protein with a molecular weight of about 180,000 (designated TSP-180) was identified that was present on line 1 cells but not on normal lung cells or Moloney sarcoma tumor cells. Studies of competition for immune precipitation of TSP-180 by unlabeled protein preparations from various sources indicate that (a) TSP-180 is present in tumor cells of various culture passage levels, (b) tumor cells grown i.m. also contain TSP-180, and (c) normal lung proteins compete weakly, and only at very high protein concentrations. A protein similar to TSP-180 was detected on Madison 109 carcinoma and on three other lung carcinomas adapted to culture. Experiments with specific antisera show that TSP-180 is not lactoperoxidase, fetal bovine serum protein, large external transformation-sensitive protein, or an antigen related to murine leukemia virus proteins.
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PMID:Characterization of a tumor cell surface protein with heterologous antisera to a spontaneous BALB/c lung carcinoma. 22 38

Differences have been observed in the kinetics of processing of the env gene polyprotein of ecotropic, xenotropic, and dual-tropic mink cell focus-forming (MCF) murine leukemia virus. In pulse-chase experiments, the env gene polyprotein of the dural-tropic MCF virus exhibits a marked increase in stability relative to that of either ecotropic or xenotropic virus. A comparison of cell surface expression of env gene products of ecotropic, xenotropic, and dual-tropic MCF murine leukemia virus has been made. Only gp70 is accessible to lactoperoxidase-catalyzed radioiodination of fibroblasts infected by ecotropic or xenotropic virus, whereas both gp70 and the env gene polyprotein are expressed on the surface of dual-tropic MCF virus-infected cells.
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PMID:Cell surface expression of the env gene polyprotein of dual-tropic mink cell focus-forming murine leukemia virus. 22 41

Haemopoietic dysplasia is a condition which often precedes the development of acute non-lymphocytic leukaemia. Before this event, however, patients are at risk from severe infections even in the absence of neutropenia. This paper describes 3 patients with haemopoietic dysplasias in whom neutrophil microbicidal activity was deficient in vitro. The important abnormality appeared to be defective release of myeloperoxidase into the phagocytic vacuole. Two of these patients suffered from numerous baterial infections.
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PMID:Neutrophil function and diagnosis of pre-leukaemic states. 22 35

Acquired myeloperoxidase deficiency has been reported in several hematological malignancies. The clinical course of a patient with acute myelomonocytic leukemia is described which was characterized by staphylococcal infections prior to therapy and again during a period of relapse. Neutropenia was not a feature of these two periods but in vitro studies revealed decreased bacterial killing capacity and decreased neutrophil myeloperoxidase activity. Infectious complications were not observed during drug-induced remission when bacterial killing capacity and myeloperoxidase activity were improved toward normal. These observations suggest that the myeloperoxidase deficient neutrophils were derived from leukemic progenitors.
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PMID:Acquired myeloperoxidase deficiency and recurrent infections in a patient with acute myelomonocytic leukemia. 22 40

Two types of apparently spontaneous malignant alterations of fibroblastlike ST/a mouse lung cells (ST-L cells) grown in vitro are described. One type is characterized by a high tumorigenic potential of the altered cells in nonconditioned syngeneic recipients, a fibroblastlike morphology with cell surface showing very few microvilli by scanning electron-microscopy (SEM), and a growth pattern typical of nontransformed cells. These cells were described as R- cells. The other type is characterized bya low tumorigenic potential in non-conditioned, immunocompetent syngeneic recipients, rounding up of the cells which by SEM showed numerous microvilli on the surface, and a growth pattern typical of transformed cells. These cells were described as round cells or R+ cells. In immunoincompetent mice, R+ cells readily produced sarcomas, which grew faster than those produced by R- cells. Both types of ST-L cells expressed murine leukemia virus (MuLV) when tested in a peroxidase anti-p30 plaque test. The concentration of murine leukemia virus envelope glycoprotein (gp70) has previously (5) been shown to be threefold higher in R+ cells compared to R- cells. Furthermore, round-cell transformation was accompanied by the development of crossreacting rejection antigens protective against a secondary shallenge with Ehrlich ascites tumor and with syngeneic dimethylbenzanthracene induced ST/a mouse leukemia (STABAL). A similar protection was obtained by preimmunization with a cloned embryonic feral mouse cell line (SC-1) infected with ST-L virus as well as with virus-free SC-1 cells, suggesting the presence of rejection antigens both of viral (gp70) and nonviral origin.
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PMID:Comparative studies of two types of "spontaneous" malignant alteration of ST/A mouse lung fibroblasts propagated in vitro. 23 Jan 49

A simple cytochemical and cytobacterial method for the simultaneous demonstration of peroxidase and lysozyme (muramidase) activities in individual cells was devised. In characterization of myeloid and monocyte series, the combination of these myeloid- and monocyte-specific enzymes not only was more informative than a single enzyme but made it easier to differentiate acute myelomonocytic leukemia, with higher lysozyme activity, from acute myeloid leukemia, with higher peroxidase activity. Acute lymphocytic leukemia had no lysozyme or peroxidase activity.
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PMID:Simultaneous demonstration of peroxidase and lysozyme activities in leukemic cells. 26 61

Leucocyte alkaline phosphatase (LAP) was histochemically detected in 7 to 18% of cells in tissue culture lines derived from the peripheral blood or bone marrow of each of 5 patients with untreated acute myelogenous or monomyelogenous leukaemia and in 30% of the cells in a clonal line of a rat promyelocytic leukaemia. Following transfer to diffusion chambers intraperitoneally implanted into total body irradiated rats, LAP levels were detected in up to 92% of human and 80% of rat leucocytes. There was no associated morphologic differentiation. In rat leukaemia cells peroxidase and myeloid specific esterase also increased from tissue culture levels. Return of cells to tissue culture decreased enzymes to pre-implant levels. Addition of plasma or peritoneal fluid from irradiated rats to cells in tissue culture again induced LAP. In contrast, LAP was not increased under these conditions with cell lines derived from patients with acute lymphatic leukaemia, or Sezary cell leukaemia. These studies indicate that a humoral factor in peritoneal fluid and plasma of irradiated rats increases LAP in human as well as rat leucocytes.
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PMID:Leucocyte alkaline phosphatase elevation in human acute leukaemia derived cell lines cultured in diffusion chambers. 26 91


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