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  • 1
    Electronic Resource
    Electronic Resource
    Selection of tumor cell variants for resistance to tumor necrosis factor also induces a form of pleiotropic drug resistance (1992)
    Springer
    Cancer immunology immunotherapy 34 (1992), S. 399-406 
    Details
    ISSN: 1432-0851
    Keywords: Tumor necrosis factor ; Pleiotropic drug resistance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary This study has addressed the question of whether there may be some common mechanism underlying the induction or expression of acquired cytokine and drug resistance in a tumor cell line. This study employed the tumor-necrosis-factor(TNF)-sensitive U937 tumor cell line as a model system to determine if selection of a tumor cell variant for cytokine resistance would also result in drug resistance and vice versa. Variants were selected by culturing in the presence of purified recombinant TNF or a mixed-lymphokine-containing supernatant derived from concanavalin-A-stimulated peripheral blood lymphocytes. The resulting variants were resistant not only to TNF, but also to certain chemotherapeutic drugs. The variants were most resistant to colchicine and theVinca alkaloids, requiring drug concentrations 50- to 5000-fold higher to mediate levels of cytotoxicity comparable to that seen with the parental U937. The variants were moderately resistant to cycloheximide, actinomycin D, and mitomycin C. In contrast, these lines were relatively sensitive to doxorubicin or daunomycin. This phenomenon was not unique to U937 cells since we obtained a similar pattern of drug resistance by selecting TNF-resistant variants of the WEHI-164 tumor cell line. The cytokine-selected U937 variants were still lysed by NK cells, although they were somewhat less sensitive than the parental U937. Both variants were relatively resistant to lysis by activated macrophages, probably because of their TNF resistance. In an alternative selection procedure, U937 variants were derived by culturing in the presence of increasing concentrations of colchicine. The resulting variants were relatively resistant to TNF, providing further support for the existence of some common mechanism operating in induction or expression of acquired cytokine and drug resistance. The resistance mechanism apparently does not involve the P glycoprotein since the cytokine-selected U937 variants do not overexpress the mdr gene. This study has demonstrated that selection of TNF-resistant variants results in coexpression of a unique form of drug resistance that is characterized by resistance to microtubule-active drugs but not to the anthracycline antibiotics and is not associated with overexpression of the mdr gene.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01741751
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  • 2
    Electronic Resource
    Electronic Resource
    Anion selectivity of apical membrane conductance of Calu 3 human airway epithelium (1999)
    Springer
    Pflügers Archiv 437 (1999), S. 812-822 
    Details
    ISSN: 1432-2013
    Keywords: Key words Anion permeation ; CFTR ; Cystic fibrosis ; Pore size ; Tight junction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Anion selectivity of the cystic fibrosis conductance transmembrane conductance regulator (CFTR) and other channels and parallel pathways expressed endogenously in apical membranes of polarized Calu-3 epithelial monolayers was studied under control conditions and during cAMP stimulation. Basolateral membranes were eliminated using alpha-toxin. The cAMP-stimulated, gradient-driven currents had the sequence Br≥Cl≥NO3〉SCN〉 I≥F〉formate〉HCO3〉acetate〉propionate=butyrate=ATP= PPi=PO4=SO4=0. Selectivity of parallel cAMP-independent pathway(s) was Br〉Cl=SCN=NO3〉I〉formate=F 〉HCO3〉acetate〉propionate. SCN, I, F or formate blocked cAMP-stimulated, but not control, Cl currents. Anions 〉0.53 nm in diameter were impermeant, suggesting that the apical CFTR channel has a limiting diameter of 0.53 nm. The selectivity, blocking patterns and pore size of the cAMP-stimulated conductance pathway were very similar to those in previous reports in which CFTR was heterologously expressed in non-epithelial cells. Thus, CFTR appears to be the major apical anion conductance pathway in Calu-3 cells, and its conduction properties are independent of the expression system. CFTR in Calu-3 cells also conducts physiologically relevant anions, but not ATP, PO4 or SO4. A pathway parallel (probably a tight junction) showed a different selectivity than CFTR.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050850
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  • 3
    Electronic Resource
    Electronic Resource
    Hepatitis E virus (HEV): Strain variation in the nonstructural gene region encoding consensus motifs for an RNA-dependent RNA polymerase and an ATP/GTP binding site (1992)
    Springer
    Virus genes 6 (1992), S. 173-185 
    Details
    ISSN: 1572-994X
    Keywords: hepatitis E ; nonstructural genes ; helicase ; viral heterogeneity ; enterically-transmitted non-A ; non-B hepatitis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hepatitis is transmitted by a number of infectious agents. The epidemiological characterization of waterborne or enterically transmitted non-A, non-B hepatitis (ET-NANBH) is unique when compared with other known hepatitides. We have reported on the molecular cloning of a cDNA clone derived from the etiologic agent associated with ET-NANBH, the hepatitis E virus (HEV). The complete sequence of these first molecular clones, isolated from an HEV-infected human after passage inMacaca fascicularis (cynomolgus macaques), illustrates a distant relationship to other known positive-strand RNA viruses of plants and animals. The translated major open reading frame (ORF-1) from these clones indicates that this portion of the genome encodes a polyprotein with consensus sequences found in RNA-dependent RNA polymerase and ATP/GTP binding domains. The latter activity has been associated with putative helicases of positive-strand RNA viruses. These viral-encoded enzymatic activities identify this region and ORF-1 as containing at least two different nonstructural genes involved in HEV replication. Molecular clones obtained from two other geographically distinct HEV isolates demonstrated sequence heterogeneity in this nonstructural gene region. Further study will be required to elucidate the pathogenic significance (if any) of this observed divergence in the nonstructural region.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01703066
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Apoptosis and DNA fragmentation precede TNF-induced cytolysis in U937 cells (1992)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 48 (1992), S. 344-355 
    Details
    ISSN: 0730-2312
    Keywords: TNF ; apoptosis ; U937 ; DNA fragmentation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The hypothesis that activation of apoptosis and DNA fragmentation is involved in TNF-mediated cytolysis of U937 tumor cells was investigated. Morphological, biochemical, and kinetic criteria established that TNF activates apoptosis as opposed to necrosis. Within 2-3 h of exposure to TNF, U937 underwent the morphological alterations characteristic of apoptosis. This was accompanied by cleavage of DNA into multiples of nucleosome size fragments. Both of these events occurred 1-2 h prior to cell death as defined by trypan blue exclusion of 51Cr release. DNA fragmentation was not a non-specific result of cell death since U937 cells lysed under hypotonic conditions did not release DNA fragments. The percentage of cells undergoing apoptosis depended on the concentration of TNF and was augmented by the addition of cycloheximide. A TNF-resistant variant derived from U937 did not undergo apoptosis in response to TNF, even in the presence of cycloheximide. Furthermore, TNF could still activate NFkB in this variant, suggesting that this pathway is not involved in TNF-mediated cytotoxicity. Two agents known to inhibit TNF-mediated cytotoxicity, ZnSo4, and 3-aminobenzamide, were shown to inhibit TNF-induced apoptosis. Taken altogether, these data support the hypothesis that activation of apoptosis is at least one essential step in the TNF lytic pathway in the U937 model system.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240480403
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