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)

Among leukemia patients, a significant number of deaths are due to Candida septicemia, many of which are associated with previous oral infections. Oral candidiasis detection methods vary, and the relationship between oral candidiasis and Candida colonization (CC) is not well defined. The main objectives of this study were to compare the incidence of CC in a healthy and leukemic population, and also to evaluate the efficacy of three simple and inexpensive methods of detecting oral CC in predicting the occurrence of oral candidiasis. A secondary objective was to portray speciation in the examined populations. Forty-two pediatric leukemia patients and 42 healthy, age-, race-, and gender-matched control patients participated in this study. The three methods of detection were cytological examination of the oral mucosa, and direct culture methods from mucosal smears using Sabouraud's dextrose agar (Becton Dickinson Microbiology Systems, Cockeysville, MD) and Oricult-N (Orion Diagnostica, Espoo, Finland). This study demonstrated an increased prevalence of CC in pediatric leukemia patients with the direct culture method detecting CC in a significantly greater proportion of the population (Oricult-N,P = 0.034; Sabouraud's dextrose agar, P = 0.0036). Candida albicans was the predominant species. Further study is needed to determine the clinical significance of oral CC and its relationship to oral candidiasis and systemic infection in pediatric leukemia patients.
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PMID:The detection of oral Candida in pediatric leukemia patients. 130 22

We have recently demonstrated that bufalin is a new potent inducer of the differentiation of human myeloid leukemia cells. The present work was carried out to examine further the effect of bufalin on the growth and characteristics of human leukemia-derived cell lines U937, ML1, and HL60. At concentrations of 5-10 nM, bufalin decreased the growth of ML1 cells preferentially at the G2 phase and U937 cells at the S and G2 phases of the cell cycle. Bufalin, under these conditions, induced the differentiation of U937, ML1, and HL60 cells to monocyte/macrophage-like cells by measuring the expression of various differentiation markers, as assessed by morphology and histochemistry, and ability to phagocytose latex particles, to reduce nitroblue tetrazolium, and to develop Fc receptors. U937 and ML1 cells started to differentiate at 4 and 6 h, respectively, after treatment with 10 nM bufalin and showed maximum differentiation 72 h later. At present, a mechanism for the bufalin-mediated induction of the differentiation of these human leukemia cells remains to be determined. The combination of bufalin with all-trans retinoic acid, 1 alpha,25-dihydroxyvitamin D3, 4'-demethylepipodophyllotoxin ethylidene-beta-D-glucoside (VP16), or human gamma-interferon synergistically induced the differentiation of HL60 and U937 cells. A similar effect on ML1 cells was observed with the combination of bufalin with VP16 or human rTNF-alpha. These results suggest that bufalin in combination with VP16, all-trans retinoic acid, 1 alpha,25-dihydroxyvitamin D3, rTNF-alpha, or gamma-interferon may be very useful in the differentiation of human leukemia.
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PMID:Induction by bufalin of differentiation of human leukemia cells HL60, U937, and ML1 toward macrophage/monocyte-like cells and its potent synergistic effect on the differentiation of human leukemia cells in combination with other inducers. 132 88

A D-galactose-specific agglutinin, named sinularian, has been isolated from the soft coral Sinularia sp. by affinity chromatography on acid-treated Sepharose 4B and by gel filtration on HPLC. Sinularian was a glycoprotein containing 11% sugar. It gave a single band corresponding to 78 kDa in SDS-PAGE, irrespective of a treatment with 2-mercaptoethanol. Sinularian agglutinated rabbit erythrocytes and murine leukemia cells but not sheep or human ABO erythrocytes. Its hemagglutinating activity was Ca(++)-independent. Sinularian promoted binding of macrophages to tumor cells.
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PMID:Purification and characterization of an agglutinin of the soft coral Sinularia species. 135 64

We devised an indicator gene for retrotransposition, nlsLacZRT, which contains the Escherichia coli lacZ gene fused to a nuclear location signal (nlsLacZ), engineered in such a way that the gene is expressed only if the structure in which it has been inserted transposes itself through an RNA intermediate. A cloned murine leukemia retrovirus with an ecotropic host range (Moloney murine leukemia virus), rendered defective by a large deletion encompassing the three viral gag, pol, and env open reading frames, was marked with this indicator gene and introduced by transfection into heterologous feline cells. No beta-galactosidase activity could be detected among the clonal cell population, unless the defective provirus was complemented in trans by the gag-pol gene products. Under these conditions, cell variants which disclosed an easily detectable nuclear blue coloration upon in situ 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside staining were observed. Fluorescence-activated cell sorting of the beta-galactosidase-positive cells, followed by Southern blot analysis, demonstrated an unambiguous correlation between nlsLacZRT activation and retrotransposition of the marked provirus. Transposition occurs at a high frequency (up to 10(-4) events per cell per generation), which is dependent on the level of expression of the gag-pol gene and is concomitant with the release of noninfectious retroviruslike particles which are the hallmarks, but not the intermediates, of the intracellular transposition process.
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PMID:High-frequency intracellular transposition of a defective mammalian provirus detected by an in situ colorimetric assay. 137 Nov 67

In the present study we examined the expression of concanavalin-A(Con-A)-like molecules on natural-killer (NK)-sensitive target cells and investigated their possible role in the human NK-cell phenomenon. The incubation of either peripheral-blood lymphocytes (PBL) or large granular lymphocytes (LGL) with swainsonine (SW), an inhibitor of mannosidase II, resulted in the augmentation of cytotoxicity against K562 leukemia cells. The enhanced cytotoxicity was associated with increased binding of fluorescein isothiocyanate-conjugated Con-A to SW-treated effector cells, and immunofluorescence staining of the target K562 cells using goat anti-Con-A antibody (Ab) showed a significant positive shift in the flow cytometric pattern. Electrophoretic separation and immunoblotting analysis revealed that 4 components with a molecular weight of approximately 95, 80, 60 and 50 kDa were recognized by anti-Con-A Ab from the detergent-extract of K562 cells. The addition of Con-A during the antibody incubation step of the Western blotting abolished their expression, thus excluding non-specific binding of the antibody. The addition of Con-A also strongly inhibited the cytotoxicity of SW-treated effector cells (PBL or LGL) against K562 cells, and this inhibition was abolished by 40 mM alpha-methyl-mannopyranoside (alpha-MM), which binds to Con-A. Furthermore, Con-A increased the binding frequency of SW-treated LGL to K562, in spite of the inhibited cytotoxicity, and this effect could be neutralized by the further addition of alpha-MM. Our results suggest that Con A-like molecules might play an important role in cell-cell interactions between SW-treated effector cells and NK target cells.
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PMID:The presence of concanavalin-A(Con-A)-like molecules on natural-killer (NK)-sensitive target cells: their possible role in swainsonine-augmented human NK cytotoxicity. 139 50

The lectin peanut agglutinin (PNA) was used to study the surface carbohydrate expression of galactose beta 1, 3, N-acetylgalactosamine by normal and malignant hemopoietic cells. Immunostaining was performed using biotinylated PNA and a streptavidin-alkaline phosphatase staining technique on 78 patients. The study was undertaken to enlarge on previous reports of lectin binding to cells of hemopoietic origin and to establish the potential role of biotinylated PNA as a component of an immunotoxin for in vitro purging of bone marrow in patients with multiple myeloma. In normals only monocytes, macrophages, centroblasts and plasma cells showed reactivity. Of the hematological malignancies, all cases of multiple myeloma were positive and non-Hodgkin's lymphoma cases with a large cell component had positive centroblasts. Two of 5 cases of acute myelomonocytic leukemia, one case of chronic myelomonocytic leukemia and one case of pleomorphic T cell non-Hodgkin's lymphoma showed PNA positive neoplastic cells. The reactivity of biotinylated PNA with centroblasts and plasma cells suggests that it may be of potential value when linked to a streptavidin-ricin conjugate in the in vitro purging of bone marrow of patients with multiple myeloma prior to autologous bone marrow transplantation.
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PMID:Peanut agglutinin (lectin from Arachis hypogaea) binding to hemopoietic cells: an immunophenotypic study using a biotin streptavidin technique. 143 89

The effect of galactose-6-mustard (G-6-M) on cell growth and cell cycle kinetics was studied in murine P388 leukemia and Chinese hamster ovary (CHO) cells in vitro and compared with the effect of L-phenylalanine mustard (L-PAM). The IC50 values of G-6-M for the P388 and CHO cells were 10 and 100 microM, respectively. No difference of the IC50 value of L-PAM (2 microM) between the two cell lines was found. The effect of G-6-M and L-PAM on cell kinetics was similar for the two cell lines at IC50 doses. The relative cell outflow from the G2 stage was inhibited to a higher extent than the relative cell outflow from the S phase. The relative cell outflow from the G1 stage was only partly inhibited. These results are discussed in relation to growth conditions, differences in DNA repair capacity, and cellular uptake of G-6-M between P388 and CHO cells.
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PMID:Comparative studies of galactose-6-mustard and L-phenylalanine mustard on cell growth and cell cycle kinetics in vitro. 152 89

Specific non-metabolizable alkyl-phospholipids selectively kill neoplastic cells, yet normal and more differentiated cells are relatively resistant. Although these highly selective anticancer lipids appear to target the cell membrane, their mechanism of cytotoxic action remains to be defined. We report here that treatment of 'sensitive' HL-60 leukemia cells with one of the most potent lipid agents, 1-alkyl-2-methoxy-glycero-3-phosphocholine, inhibits the cellular transport of multiple essential nutrients including choline, amino acids, fatty acids, and the non-metabolizable carbohydrate, 2-deoxy-D-glucose. Minimal inhibitory responses of the varied transport systems were noted in HL-60 cells treated with the less potent, 2-lyso analog, and in 'resistant' K562 leukemia cells, treated with the 2-methoxy lipid. Although both the 2-methoxy lipid and 12-tetradacanoylphorbol 13-acetate induce differentiation in HL-60 cells, significant differences in the interactions of these lipids on cellular choline transport were found. Based on these results, we conclude that multiple nutrient deprivation induced by the detergent-like action of the methoxy-containing alkyl phospholipid results in the selective destruction of neoplastic cells that are sensitive to this membrane-targeted antitumor agent.
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PMID:Inhibition of cellular transport systems by alkyl phospholipid analogs in HL-60 human leukemia cells. 162 36

beta-D-galactose-containing glycoproteins were prepared from cells P-388 leukemia and from P-388 leukemia cells with induced resistance to doxorubicin. It was shown by HPLC method that plasma membranes from resistant cells contain 4-4.5% P-glycoproteins and plasma membranes from sensitive cells contain P-glycoproteins about 10 times lower.
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PMID:[The expression of P-glycoprotein in leukemia P388 cells with induced doxorubicin resistance]. 167 97

A retrovirus promoter-trap vector (U3LacZ) has been developed in which Escherichia coli lacZ coding sequences were inserted into the 3' long terminal repeat (LTR) of an enhancerless Moloney murine leukemia virus. The U3LacZ virus contains the longest reported LTR (3.4 kbp); nevertheless, lacZ sequences did not interfere with the ability of the virus to transduce a neomycin resistance gene expressed from an internal promoter. Duplication of the LTR placed lacZ sequences in the 5' LTR just 30 nucleotides from the flanking cellular DNA. Approximately 0.4% of integrated proviruses expressed beta-galactosidase as judged by 5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside (X-Gal) staining, and individual clones expressing lacZ were isolated by fluorescence-activated cell sorting. In all clones examined, beta-galactosidase expression resulted from the fusion of lacZ sequences to transcriptional promoters located in the flanking cellular DNA. Furthermore, by differential sorting of neomycin-resistant cell populations, clones were isolated in which lacZ expression was induced and repressed in growth-arrested and log phase cells, respectively.
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PMID:Retrovirus promoter-trap vector to induce lacZ gene fusions in mammalian cells. 170 29


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