Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023467 (acute myeloid leukemia)
 35,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

G-banding of chromosome metaphase preparations derived from haemic cells of healthy individuals and from patients with acute myeloid leukaemia was performed with the aid of trypsin, papain, and pretreatment of the chromosome spreads with emulphogene before proteolytic digestion. Papain digestion revealed more distinguishable bands than did trypsin digestion. Pretreatment of the chromosome spreads with emulphogene greatly enhanced the number of distinguishable bands for both enzymes. The combination of pretreatment with emulphogene and digestion with papain revealed optimal numbers of bands for individual chromosomes essentially identical with those agreed at the Paris Conference 1971. The use of the emulphogene-papain technique appears also to offer an advantage in the banding of chromosomes from leukaemic cells.
 ...
PMID:A comparative study of chromosome G-banding using trypsin, papain, and pretreatment with emulphogene. 28 44

Peripheral blood leukocytes from 31 out of 48 patients with acute myelogenous leukemia grew in short-term liquid culture. Two distinct types of growth occurred. The first type was dimorphic with supernatant free-floating ("non-sticker") cells and, in addition, a plastic/glass adherent, trypsin resistant, phagocytic population ("stickers"). The second type which occurred less frequently than the first consisted almost entirely of free-floating "non-sticker" cells. Although patients with this second type of growth pattern almost invariably had AML, 44% of AML's produced monocytoid "sticker" cells in culture. Cells from the majority of patients with ALL did not grow in culture.
 ...
PMID:Morphological characterisation of adult acute leukaemia in short-term liquid culture. 107 63

Chromosome studies were carried out after a 24-hour harvest of unstimulated bone marrow aspirate cell cultures from a 75-year-old male with a clinical diagnosis of acute myelomonocytic leukemia (FAB M4). Analysis of nine cells after trypsin-Giemsa banding (GTG) revealed two cell lines with a mosaic chromosome pattern, 46,XY/46,XY,t(7;19)(q22;p13.3). A review of the recent literature reveals one case of childhood ALL with a 46,XY/46,XY,t(7;19)(q11;q13) chromosome pattern [1] and a 46,XY,t(3q;11q),t(7q;19p),t(15;17)(q26;q22) in one patient with ANLL (FAB M3) [2]. The t(7;19)(q22;p13.3) seen in our case has not been reported as the sole specific clonal chromosome rearrangement in myeloid neoplasia. Interestingly, the plasminogen activator inhibitor type I, multi-drug resistance, and erythropoietin genes are located at band 7q22 and the insulin receptor gene is located at band 19p13.3. Both sites contain fragile site loci. The possible role of these fragile sites, genes, or other genes in the rearrangement can only be surmised.
 ...
PMID:Atypical (7;19) translocation in acute myelomonocytic leukemia. 175 94

We examined activities of procoagulant and fibrinolysis in homogenate of leukemic cells. Procoagulant activity (PCA) was increased in patients with acute myelocytic leukemia (AML) and acute promyelocytic leukemia (APL), but it was significantly decreased in patients with chronic myelocytic leukemia (CML) and adult T cell leukemia. In CML, PCA was increased in the blastic phase. Plasminogen activator activity (PLGAA) was also increased in patients with AML, APL and acute lymphocytic leukemia (ALL) associated with disseminated intravascular coagulation (DIC). Elastase-like activity, trypsin-like activity and chymotrypsin-like activity (CTLA) were increased in those with myelocytic leukemia, but they were low in those with lymphocytic leukemia. PCA, PLGAA and CTLA were significantly higher in patients with DIC than in those without DIC. Measurement of procoagulant and fibrinolytic activity in leukemic cells homogenate may be useful not only for studying hemostatic abnormalities but also for classification of leukemic cells.
 ...
PMID:[Activity of procoagulant and fibrinolysis in homogenate of leukemic cells]. 259 44

Four monoclonal antibodies against human erythrocyte membrane antigens were established. The antigenic determinants of KOR-E1, E3, E6 were Pr1h antigen, Wrb antigen, and the trypsin sensitive portion of glycophorin A (EnaTS) respectively. The antigen recognized by KOR-E4 could not be determined. The reactivities of these antibodies with normal hematopoietic cells, malignant hematopoietic cell lines (N = 31), and fresh leukemic cells obtained from 128 patients with various types of leukemias were studied. All antibodies reacted only with erythrocytes among peripheral blood cells, and also KOR-E6 reacted only with erythroid cells among bone marrow cells. KOR-E3 had no reactivity with any cell lines examined, and KOR-E1 and KOR-E4 were reactive with some lymphoid cell lines. However, KOR-E6 had specific reactivities with erythroid (HEL, K562), megakaryocytic (CMK-1), multiphenotypic (KOPM-28), and basophilic (KU-812) cell lines. The antigen (glycophorin A) recognized by KOR-E6 was expressed on a small population of mononuclear cells separated from acute lymphoblastic leukemia (3/70), acute myelogenous leukemia (2/12), monosomy 7-myeloproliferative disorder (1/1), juvenile CML (1/1), and transient myeloproliferative disorder with Down's syndrome (4/12), although it could not be determined whether these cells were leukemic cells or not. KOR-E6 was reactive with a large population of leukemic blasts in erythroleukemia (2/2) and acute megakaryoblastic leukemia (3/6). Thus, KOR-E6 appears to be an erythroid marker of leukemic cells.
 ...
PMID:[Monoclonal antibodies against human erythrocyte membrane antigens and their reactivities with hematopoietic cells]. 261 36

Leukemia associated inhibitor, LAI, reversibly inhibits DNA synthesis in normal human granulocyte-macrophage colony-forming units (CFU-GM). LAI is produced by myeloid leukemia cells, a subpopulation of normal nonadherent low-density mononuclear cells in peripheral blood and bone marrow, as well as by the human promyelocytic cell line HL-60. Normal low-density marrow cell absorbed LAI at 37 degrees C from HL-60 cell-conditioned medium. When normal marrow cells were treated with trypsin or chymotrypsin they lost their capacity to absorb LAI and also became insensitive to the inhibitory effect of LAI. These observations were taken as circumstantial evidence for the existence of a trypsin-sensitive LAI receptor on normal marrow cells, including CFU-GM. Glucocorticoid steroids (hydrocortisone, prednisolone, and dexamethasone) inhibited LAI production by acute myeloid leukemia (AML) cells, normal LAI-producing cells, and HL-60 cells. The fact that prostaglandin E1 (PGE) totally inhibited LAI production by normal cells and that indomethacin abrogated the inhibitory effect of adherent cells on LAI production suggested a role for adherent monocytic cells and PGE in the regulation of LAI production.
 ...
PMID:Modulation of the production of leukemia associated inhibitor (LAI) and its interaction with granulocyte-macrophage colony-forming cells. 350 70

Cytogenetic analyses by means of trypsin-Giemsa banding technique were performed on bone marrow cells from a total of 12 patients--nine with acute nonlymphocytic leukemia and three with myelodysplastic syndrome--and a history of rheumatoid arthritis. Clonal chromosomal abnormalities were identified in two patients with previous exposure to petroleum products, and radiation therapy for a malignant tumor, respectively; one additional patient had a loss of the Y chromosome as the sole aberration. All the remaining nine patients had completely normal karyotypes. Seven patients had received treatment for rheumatoid arthritis with mutagenic drugs. Acute nonlymphocytic leukemia or myelodysplastic syndrome secondary to cytotoxic treatment for a previous malignancy display multiple, usually complex, structural and numerical chromosomal abnormalities in the majority of cases. The contrasting findings in the present patient series suggest other pathogenetic mechanisms in acute nonlymphocytic leukemia and myelodysplastic syndrome following rheumatoid arthritis.
 ...
PMID:Normal bone marrow karyotype in acute leukemia or myelodysplasia following rheumatoid arthritis? 380 51

Exogenous serine proteases were found to induce differentiation in human myeloid leukemic cells from either in vitro established long-term cell lines or in primary cultures of cells derived directly from patients with acute myeloid leukemia. Exposure of the human promyelocytic cell line HL-60 to trypsin, chymotrypsin, or elastase induced the appearance, within 3-6 days, of neutrophilic granulocytes defined by their morphology, their ability to reduce nitroblue tetrazolium, and their efficient phagocytosis of latex particles. Upon further incubation monocyte-like cells appeared. While these cells developed into fully mature macrophages other types of cells disappeared and on day 12 the culture consisted of a pure macrophage population. The inducing effect could be observed when the enzyme was presented alone, whereas a synergistic effect was noted when the protease was added in the presence of subthreshold concentrations of chemicals known to induce differentiation in this cell line such as dimethylsulfoxide, retinoic acid, butyric acid, or hexamethylene bisacetamide. Optimal induction of differentiation by trypsin required a 48 hr continuous exposure to the enzyme. When the protease was removed earlier no appreciable differentiation was noticed. The protease-induced differentiation involved a direct interaction with the cells and was not due to a proteolytic cleavage of a serum component because it could be obtained in serum-free cultures. The enzymatic activity of the protease was needed for its effect on cell maturation: Addition of protease inhibitors such as soybean-trypsin inhibitor or trasylol completely blocked differentiation induced by the proteases but had no effect on differentiation induced by the other inducers. It is still to be determined whether a proteolytic process is a general molecular event in cell differentiation or induction by chemicals involves a mechanism different from that initiated by exogenous proteases.
 ...
PMID:Induction of differentiation in human myeloid leukemic cells by proteolytic enzymes. 388 35

To examine the plasma membrane characteristics of an immature monocytic cell capable of proliferation, we have developed a murine monoclonal antibody that identifies an antigen, Mb1, found on the surface of U-937. In immunofluorescence analyses, Mb1 is not expressed by peripheral blood monocytes (freshly isolated, lymphokine-activated, or cultured for seven days), neutrophils, or any other circulating element. It is also absent on human bone marrow mononuclear cells, including the CFU-GM. Among a series of malignant cells from 50 patients with acute myeloid leukemia (including 22 with monocytic or myelomonocytic leukemia), no Mb1 expression was detected. Continuous human cell lines of B or T cell origin were also negative, as were the myeloid lines HL-60 and K562. Apart from U-937, which uniformly expresses Mb1 in high antigen density, only KG-1 (a myeloblastic line) exhibits Mb1 in low antigen density. Exposure of U-937 to phorbol diester (TPA) under conditions that induce features of macrophage differentiation (including the expression of Mo1) results in a significant reduction in Mb1 expression. Mb1 expression is also reduced as a result of culture of U-937 in medium containing anti-Mb1 antibody (antigenic modulation). On sodium dodecyl sulfate-polyacrylamide gel electrophoresis of radiolabeled immunoprecipitates, Mb1 appears to be a dimeric protein with an estimated molecular weight of 80 kd (43 kd under reducing conditions). Antigenic activity on U-937 is destroyed by treatment with trypsin or papain but is regenerated after 24 hours' culture in enzyme-free medium. Mb1 is a constituent plasma membrane protein of U-937, and its degree of expression relates to the state of cellular differentiation.
 ...
PMID:Mb1, a plasma membrane antigen selectively expressed by U-937 cells. 389 Sep 83

We studied the ability of untreated or immunoadsorbed acute myelogenous leukemia (AML) sera to kill AML blasts. Culture of blasts with sera adsorbed to protein A-bearing Staphylococcus aureus Cowan I (SAC), resulted in a marked loss of blast viability (42.7% of control). Immunoadsorption against non-protein A-bearing Wood 46 strain of S. aureus did not induce serum cytotoxic activity (94.8% viable cells). Sera adsorbed to Sepharose-bound protein A also killed blasts in vitro (64.3% viable cells). The addition of untreated sera to SAC-treated cultures partly abrogated the effect, suggesting a blocking substance in untreated serum. Cytotoxicity was not complement-dependent nor did it appear to be cell mediated. It was, however, eliminated by trypsin treatment of SAC-treated sera. These studies suggest that SAC-treated AML serum contains a protein that is cytotoxic to AML blasts, and that this protein is partly inactivated by untreated AML serum, possibly through interaction with immunoglobulins. The mechanism described here may be one of several mechanisms leading to tumor necrosis in tumor-bearing hosts treated with SAC-immunoadsorbed plasma.
 ...
PMID:In vitro tumoricidal activity of immunoadsorbed leukemic serum. 637 6


1 2 3 4 5 Next >>