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)

The effects of hot-water extract of pine cone (PCE) of Pinus parviflora Sieb. et Zucc. on the growth and differentiation of ML-1 cells, derived from a patient with human myeloblastic leukemia, were investigated. Growth of ML-1 cells was slightly inhibited at 3% (v/v) PCE, and a cytotoxic effect appeared at greater than 10%. Growth inhibition was accompanied by conversion to morphologically macrophage-like cells with alpha-naphthyl acetate esterase activity. In contrast, PCE dose-dependently increased the Fc receptor and nitroblue tetrazolium (NBT)-reducing activity up to 3%; above 3% its effect declined. Most of the cytotoxic activity was extracted from PCE with ethanol, and separated from the insoluble pellet, which contained the differentiation-inducing activity. The differentiation-inducing activity was eluted near the void volume on Sephadex G-200 gel filtration, with a 260-fold increase in the specific activity.
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PMID:Partial purification of novel differentiation-inducing substances(s) from hot water extract of Japanese pine cone. 308 16

A method using flow cytometry and fluorescent in situ hybridization (ISH) to detect RNA in cells is described. L1210 murine leukemia cells were fixed with 1% formaldehyde in HEPES buffered Hank's balanced salt solution (HH) followed by 70% ethanol. Endogenous RNAses were blocked by diethylpyrocarbonate treatment. Single-stranded sense and antisense RNA probes, labeled with biotin-11-UTP, were transcribed from a 2.1 kb 28S ribosomal RNA (rRNA) gene fragment subcloned into the pGEM2 plasmid. For good results, it was essential that the probes were degraded to 100-150 nucleotides before use. Hybridization was performed at 45 degrees C in 50% formamide, 5 x SSC, 0.5% SDS. Hybrids were detected with streptavidin-FITC by flow cytometry. Antisense rRNA probe signal was 100 times higher than the background. The hybrids were largely resistant to RNAse and melted at high temperature. The sense probe also gave a signal (5 times background), which was not RNAse resistant and was attributed to the presence of internal inverted repeats in the ribosomal RNA. When sufficient background reduction can be achieved, it is expected that as few as ten mRNA molecules per cell can be detected with the fluorescent in situ hybridization method.
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PMID:Flow cytometric detection of ribosomal RNA in suspended cells by fluorescent in situ hybridization. 320 17

We have employed ethanol-fixed wax embedded sections of human breast tumours and smears of rat leukaemia cells to provide test systems with recognisable tumour cells amongst normal cells. We have used 9-aminoacridine to locate cells possesing guanidinobenzoatase, an enzyme which degrades fibronectin and which binds 9-aminoacridine to its active centre. The binding of 9-aminoacridine to tumour cells allows these cells to be located by fluorescent microscopy. Pre-treatment of these sections with BZAR, a known inhibitor of guanidinobenzoatase inhibited the binding of 9-aminoacridine to the tumour cells. These techniques defined the tumour cells in the sections; we then demonstrated by fluorescent microscopy that both Texas red-agmatine and BZAR also bound to the guanidinobenzoatase of these tumour cells. These fluorescent probes have been used as model compounds to illustrate the ability of both N-substituted agmatines and N-substituted arginines to deliver desired molecules to an enzyme on the surface of tumour cells. Replacement of these fluorescent moieties by cytotoxic moieties attached to the same ligands could lead to selective drug delivery to tumour cells.
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PMID:A fluorescent study of ligands for guanidinobenzoatase, a protease associated with tumour cells. 321 54

Immunoglobulin samples (HIV-Ig) were prepared by cold ethanol fractionation of human plasma containing antibody against human immunodeficiency virus (HIV). The ability to prevent viral spreading was studied using either human T-cell leukemia virus type I (HTLV-I)-carrying MT-4 cells or in a coculture system using MOLT-4 cells and virus-producing MOLT-4/HIV HTLV-IIIB cells. Treatment of HIV-infected MT-4 cells with HIV-Ig effectively blocked the appearance of antigens of HIV and the virus-induced cytopathic effect. HIV-Ig blocked multinucleated giant cell formation in the MOLT-4 and MOLT-4/HIV HTLV-IIIB coculture system.
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PMID:Efficacy of an immunoglobulin preparation from HIV carriers in preventing HIV replication in vitro. 336 35

A monoclonal antibody (mAb) with framework reactivity against the T cell receptor (TCR) alpha beta complex is characterized. The mAb, beta Framework 1 (beta F1) is capable of immunoprecipitating the TCR alpha beta complex from 125I-labeled human T cell tumors, immunocompetent T cell clones, and peripheral blood lymphocytes (PBL). beta F1 recognizes the separated TCR beta subunit in Western blotting. Because it does not bind to the surface of viable T cells but does react with the plasma membrane form of the TCR after treatment with membrane solubilizing agents, the beta F1 mAb reacts with a "hidden" determinant on the TCR beta subunit. After solubilization with 70% ethanol, the TCR alpha beta complex is shown to exist on greater than 92% of T3+ human PBL, whereas 2 to 8% of T3+ PBL do not react with the mAb. The beta F1 mAb demonstrates the existence of differently glycosylated surface 125I-labeled TCR alpha-chains (alpha, alpha', alpha") in association with a common TCR beta-chain on the HPB-MLT T cell leukemia. Reactivity of the beta F1 mAb on thymus tissue sections is similar to that of anti-Leu-4 (anti-T3). The beta F1 mAb should prove useful as a research tool for both the immunochemical characterization and isolation of virtually any alpha beta T cell receptor, whether from individual T cell clones or polyclonal populations of T lymphocytes. Recognition of T cell receptors in histologic tissue sections suggests that the beta F1 mAb may be useful in the clinical diagnosis of T cell lineage neoplasms. In failing to recognize all T3+ lymphocytes, it allows the identification of novel populations of T3+ lymphocytes that may express non-alpha, non-beta T cell receptors.
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PMID:Characterization and expression of the human alpha beta T cell receptor by using a framework monoclonal antibody. 349 55

A pharmacokinetic study was performed in 13 adult patients with acute nonlymphoblastic leukemia to compare two formulations of 4'-(9-acridinylamino)-methanesulphone-m-ansidide (AMSA): the original formulation, AMSA-NCL, and a water-soluble lyophilized formulation, AMSA-lactate (Bristol Myers, Syracuse, N.Y. USA). Initially, the patients received either AMSA-NCL or AMSA-lactate, 75-90 mg/m2 daily, for 3-7 days as a 1-h infusion. Eight patients subsequently crossed over to receive the other formulation. Plasma samples for drug determination were collected during the first 3 days. A new method for determination of AMSA is described. Acidified plasma samples containing an internal standard were extracted with hexane, then made alkaline, whereafter, AMSA was extracted with ethylacetate. Extracts were reconstituted in absolute ethanol and analyzed by high-pressure liquid chromatography (HPLC) using a reverse-phase C-18 column and UV detection at 254 nm. There were no clear differences in clinical effects and toxicity between the two formulations. Patients with the highest total area under the drug concentration-versus-time curves (AUCs) for plasma concentrations versus time had significantly lower nadir for white blood cell count, suggesting a relation between plasma levels and bone marrow toxicity for AMSA. The pharmacokinetics showed a biphasic elimination for both formulations. The mean terminal elimination half-life of AMSA-NCL and AMSA-lactate was 7.1 and 6.3 h, respectively, and the mean volume of distribution was 105 and 99 L/m2, respectively. No significant differences in the pharmacokinetics comparing days 1 and 3 were seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of the pharmacokinetics of AMSA and AMSA-lactate in patients with acute nonlymphoblastic leukemia. 367 68

On the consideration that the highly active DNA-nonbinding adriamycin analogues N-(trifluoroacetyl)adriamycin 14-valerate and N-(trifluoroacetyl)adriamycin 14-O-hemiadipate undergo initial metabolic conversion to N-(trifluoroacetyl)adriamycin by the action of nonspecific serum and tissue esterases, a number of N-(trifluoroacetyl)adriamycin 14-thio esters have been prepared and studied for in vitro growth inhibition, vs. human-derived CCRF-CEM leukemic lymphocytes, and in vivo antitumor activity, vs. murine P388 leukemia, relative to the rate of thio ester deacylation induced by esterases present in mouse serum. Products were obtained by reaction of N-(trifluoroacetyl)-14-bromodaunorubicin with thioacetic, thiopropionic, thiobutyric, thiovaleric, and thiobenzoic acids in ethanol, in the presence of potassium carbonate. Because little is known about similar thio ester derivatives of adriamycin itself, the corresponding adriamycin 14-thio esters were also prepared and evaluated for antitumor activity; with these products, determination of their extent of interaction with calf thymus DNA was also performed. For the adriamycin thio ester products, significant in vivo anti-P388 activity was seen with the thioacetate, thiovalerate, and thiobenzoate derivatives, although no compound matched the curative effects of N-(trifluoroacetyl)adriamycin 14-valerate in this system. With respect to the N-(trifluoroacetyl)adriamycin 14-thio ester products, although the corresponding oxo ester analogues are all significantly biologically active, none of the thio ester derivatives showed activity in vitro or in vivo.
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PMID:Adriamycin analogues. Preparation and biological evaluation of some thio ester analogues of adriamycin and N-(trifluoroacetyl)adriamycin 14-valerate. 380 75

Australia antigen [Au(1)], a particle associated with viral hepatitis, was isolated from the plasma of a patient with chronic anicteric hepatitis and leukemia who had received radioactive phosphorus. We have found that the immunoreactivity and appearance of Au(1) in the electron microscope were not altered by treatment with enzymes including trypsin, pronase, lipase, phospholipase C, ribonuclease, deoxyribonuclease, amylase, and neuraminidase. In contrast, other serum constituents were degraded by these enzymes. Therefore, treatment of the patient's plasma with many enzymes was exploited as an initial step for the isolation of Au(1). Subsequently, Au(1) was purified from the enzyme-treated (32)P-labeled plasma by gel filtration through Sephadex G-200 and centrifugation through sucrose and in cesium chloride gradients. There were no detectable human serum components in the purest fractions, as tested by immunoelectrophoresis and immunodiffusion. The density of the purified Au(1) was 1.21 in CsCl. The particle measured about 200 A in diameter, was predominantly spherical in shape and appeared to be composed of subunits. Nucleic acids were not detected by spectrophotometric, radiochemical, and chemical analyses. Immunoreactivity of purified Au(1) was destroyed by heating for 1 hr at 85 degrees C but was stable at 56 degrees C. Treatment with Carnoy's solution (3 parts ethanol:1 part glacial acetic acid) followed by pronase disrupted the particles as seen with the electron microscope. These findings, combined with other published information on Australia antigen and viral hepatitis, suggest that the bulk of Australia antigen in the blood of this patient is an incomplete virus or virus capsid.
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PMID:Australia antigen (a hepatitis-associated antigen): purification and physical properties. 424 40

A staining procedure is described for quantitative analysis of cellular RNA content distributions by flow cytometry (FCM). Cells were fixed in ethanol, treated with DNAse and stained with propidium iodide. FCM analysis showed that more than 90% of the fluorescence resulted from the double-stranded RNA (dsRNA) bound fluorochrome. The dsRNA content distributions were measured in HeLa S3 cells in culture 24-120 hr after plating, in L1210 ascitic leukemic cells 1-7 days after transplantation, and in regenerating bone marrow 3-7 days after injection of cyclophosphamide. In all three cell populations, maximal dsRNA content was observed during the period of most active cell proliferation, as determined by the S-phase index derived from the DNA histograms. In the dsRNA distributions in L1210 leukemia cell populations 1-2 days after transplantation, two separate peaks were evident, representing weakly fluorescent, presumably nontumor cells, and intensively fluorescent tumor cells. The amount of dsRNA-bound fluorochrome was significantly greater in L1210 cells than in normal and regenerating bone marrow cells and also greater in spontaneous thymic lymphoma cells than in normal thymic cells.
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PMID:Flow cytometric analysis of double-stranded RNA content distributions. 615 1

The plasma concentration of beta-thromboglobulin was serially measured in nine patients with septicemia, ten patients with pneumonia and five thrombo- and granulocytopenic patients with acute leukemia. Six patients with septicemia out of the eight studied on days 1-3 and all eight patients studied 7-14 days after onset had an abnormal high beta-thromboglobulin level. One patient with pneumonia out of six studied on days 1-3 and six out of nine studied on 7-14 days after onset had an abnormal high value. A rising trend in plasma beta-thromboglobulin with the highest mean levels at one to two weeks after onset was common to both groups. Positive ethanol gelation, increased level of fibrin/fibrinogen degradation products, decreased antithrombin III, increased FVIII complex and disproportionate ratio of FVIII:C to FVIIIR:Ag were common in both groups in the early stages of the disease. All the five patients with leukemia had a lower than normal beta-thromboglobulin level throughout the study but showed in the coagulation parameters changes similar to those observed in the other groups. Judging from the commonness of abnormal beta-thromboglobulin values in the two first patient groups, low grade platelet activation is a normal response in severe infection.
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PMID:Plasma beta-thromboglobulin in severe infection. 618 May 2


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