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  • 1
    Electronic Resource
    Electronic Resource
    Current concepts and controversies in chemical carcinogenesis (1981)
    New York, NY : Wiley-Blackwell
    Journal of Supramolecular Structure and Cellular Biochemistry 17 (1981), S. 99-120 
    Details
    ISSN: 0275-3723
    Keywords: Chemistry ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jsscb.380170202
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  • 2
    Electronic Resource
    Electronic Resource
    Action of phorbol esters in cell culture: Mimicry of transformation, altered differentiation, and effects on cell membranes (1979)
    New York, N.Y. : Wiley-Blackwell
    Journal of Supramolecular Structure 12 (1979), S. 195-208 
    Details
    ISSN: 0091-7419
    Keywords: tumor promoters ; phorbol esters ; plasminogen activator ; epidermal growth factor ; carcinogenesis ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The carcinogenic process is usually multifactor in its causation and multistep in its evolution. It is likely that entirely different molecular mechanisms underlie the many steps in this process. In contrast t o initiating carcinogens, the action of the tumor-promoting phorbol esters does not appear t o involve covalent binding t o cellular DNA and they are not mutagenic. Recent studies in cell culture have revealed two interesting biologic effects of the phorbol esters and related macrocyclic plant diterpenes. The first is that at nanomolar concentrations they induce several changes that resemble those seen in cells transformed by chemical carcinogens or tumor viruses. These include altered morphology and increased saturation density, altered cell surface fucose-glycopeptides, decrease in the LETS protein, increased transport of deoxyglucose, and increased levels of plasminogen activator and ornithine decarboxylase. In transformed cells exposed to phorbol esters the expression of these features is further accentuated. Phorbol esters do not induce normal cells to grow in agar but they do enhance the growth in agar of certain transformed cells. The second effect of the phorbol esters is inhibition of terminal differentiation. This effect extends to a variety of programs of differentiation and is reversible when the agent is removed. With certain cell culture systems induction of differentiation, rather than inhibition, is observed. Both the transformation mimetic and the differentiation effects are exerted by plant diterpenes that have tumor-promoting activity but not by congeners that lack such activity. The primary target of phorbol esters appears to be the cell membrane. Early membrane-related effects include enhanced uptake of 2-deoxyglucose and other nutrients, altered cell adhesion, induction of arachidonic acid release and prostaglandin synthesis, inhibition of the binding of epidermal growth factor t o cell surface receptors, altered lipid metabolism, and modifications in the activities of other cell surface receptors. A model of “two stage” carcinogenesis encompassing the known molecular and cellular effects of initiating carcinogens and tumor promoters is presented. According to this model, initiating carcinogens induce stable alterations in the cellular genome but these are not manifested until tumor promoters modulate programs of gene expression and induce the clonal outgrowth of the initiated cell.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jss.400120206
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  • 3
    Electronic Resource
    Electronic Resource
    Phenotypic effects of overexpression of PKCβ1 in rat liver epithelial cells (1989)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 41 (1989), S. 179-188 
    Details
    ISSN: 0730-2312
    Keywords: protein kinase C ; TPA ; cell transformation ; gene expression ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: We have used a previously described retroviral expression vector pMV7-PKCβ1 to develop derivatives of two rat liver epithelial cell lines, K16 and K22, that stably express about tenfold-higher PKC activity than control cells. Despite these high levels of PKC, these cells did not exhibit gross morphologic changes, anchorage-independent growth, or tumorigenicity. K16PKC-4 and K22PKC-2, two lines with the highest PKC enzyme activity, were studied further in terms of several responses to the phorbol ester tumor promoter TPA. When treated with 100 ng/ml of TPA, the control K16MV7 and K22MV7 cells displayed a slight change in morphology, whereas the K16PKC-4 and K22PKC-2 cells displayed a marked change in morphology. Northern blot analyses demonstrated that TPA induced increased levels of fos, myc, phorbin, and ODC RNAs in control K16MV7 and K22MV7 cells, with maximum induction occurring at about 0.5, 1, 8, and 8 h, respectively. In K16PKC-4 and K22PKC-2 cells, TPA induction of phorbin and ODC RNAs was markedly enhanced, but this was not the case for myc and fos RNAs. In addition, the levels of myc RNA were constitutively higher in both K16PKC-4 and K22PKC-2 cells than in the control cells. Taken together, these results provide direct evidence that PKC plays a critical role in modulating the expression of myc, phorbin, and ODC RNAs. On the other hand, overexpression of PKCβ1 is not itself sufficient to cause cell transformation.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240410403
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  • 4
    Electronic Resource
    Electronic Resource
    Growth factors, oncogenes, and multistage carcinogenesis (1987)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 33 (1987), S. 213-224 
    Details
    ISSN: 0730-2312
    Keywords: protein kinases ; protein kinase C ; interferon ; phorbol esters ; tumor promotion ; signal transduction ; growth factors ; oncogenes ; multistage carcinogenesis ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: This paper presents evidence that the full repertoire of cellular genes involved in the carcinogenic process is several times larger than that of the known list of proto-oncogenes. Furthermore, this repertoire includes genes whose normal function is related to growth stimulation, as well as genes whose normal function is to inhibit growth or induce terminal differentiation. Multistage carcinogenesis probably results from a complex series of changes in both categories of genes. Despite this complexity, carcinogenesis can be conceived in terms of disturbances in biochemical functions that normally control the expression or function of growth factors, receptors, and pathways of signal transduction. Several protein kinases play a central role in the process of signal transduction. Our laboratory has recently isolated cDNA clones for the enzyme protein kinase C (PKC). These clones should be useful for clarifying the role of PKC in growth control and tumor promotion. Finally, the existence of genes whose normal function is to inhibit cell growth provides a rationale for new strategies of cancer prevention and treatment.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240330308
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  • 5
    Electronic Resource
    Electronic Resource
    Relevance of cyclin D1 and other molecular markers to cancer chemoprevention (1996)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 63 (1996), S. 23-28 
    Details
    ISSN: 0730-2312
    Keywords: cancer ; cell cycle ; chemoprevention cyclins ; markers ; prevention ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Until recently studies on mutations in cellular genes implicated in multistage carcinogenesis have concentrated mainly on dominant acting mutations in cellular proto-oncogenes, genes that normally mediate agonist-induced signal transduction pathways, and recessive mutations in cellular tumor suppressor genes, whose normal products appear to inhibit cell growth and/or control differentiation and cell-cell interactions. It seems likely, however, that a third category of cellular genes, the cyclins and cyclin-related genes, may also be critical targets during multistage carcinogenesis because of the central role that they play in controlling cell cycle progression. These proteins could, therefore, provide biomarkers for identifying individuals at high risk of developing cancer and also serve as novel targets for chemopreventive agents. This paper reviews evidence that the gene cyclin D1 is amplified and/or overexpressed in a major fraction of human tumors, and that this can occur relatively early in the carcinogenic process. Mechanistic studies indicates that this overexpression plays a critical role in tumor progression as well as the maintenance of the tumorigenic phenotype. Thus, increased cyclin D1 expression can enhance gene amplification and cell transformation and antisense to cyclin D1 can revert malignant cells. The latter findings provide direct evidence that cyclin D and related proteins might be useful markers and also targets for cancer chemoprevention. J. Cell. Biochem. 25S:23-28. © 1997 Wiley-Liss, Inc.
    Additional Material: 1 Ill.
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  • 6
    Electronic Resource
    Electronic Resource
    Isolation and charactrization of a morphologic variant of chinese hamster (CHO) cells (1980)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 102 (1980), S. 141-153 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: An epithelioid clone of Chinese hamster (CHO) cells which is spontaneously transformed was exposed to the mutagen N-methyl-N-Nitro-N-Nitrosoguanidine (MNNG), and a fibroblastic variant, clone CHO-F2, was isolated. This clone is partially reverted in several of the in vitro properties characteristic of transformed cells. When compared to wild type CHO, CHO-F2 has a longer doubling time, a lower saturation density and less piling up at high cell density, and a higher serum requirement. CHO-F2 also elaborates less plasminogen activator and has more abundant microtubules and actin cables. On the other hand, both CHO and CHO-F2 grow in agar suspension (although CHO-F2 grows with a lower efficiency), both lack detectable LETS protein, and both are tumorigenic in nude mice. Thus, expression of the individual properties frequently associated with transformation and tumorigenicity can be dissociated.The most critical biochemical change in CHO-F2 appears to bean increase in the intracellular level of cyclic AMP, when compared to CHO, and several growth and morphological properties of CHO-F2 resemble those induced in wild type CHO exposed to exogenous dibutyryl cyclic AMP. Therole of cyclic AMP in expression of the transformed phenotype and the significance of individual in vitro parameters of transformation with respect to tumorigenicity are discussed.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041020206
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  • 7
    Electronic Resource
    Electronic Resource
    Effects of mevinolin and mevalonate on cell growth in several transformed cell lines (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 127 (1986), S. 216-222 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Studies were conducted to explore the effects of mevinolin, a competitive inhibitor of HMG CoA reductase, on the growth and morphology of normal and transformed murine fibroblasts. Mevinolin is known to block DNA synthesis and cell growth in a number of kinds of non-transformed cells. Eight cell lines were studied, including two normal fibroblast cell lines (C3H 10T 1/2 and NIH 3T3) and derivatives of these cell lines transformed by chemical carcinogens, X-irradiation or the H-ras oncogene. All of the eight cell lines displayed appreciable growth inhibition by 5 μM mevinolin and marked inhibition by 30 μM mevinolin. Mevinolin also induced a marked rounding in the morphology of all of the cell lines. These effects of mevinolin on cell growth and morphology were blocked or reversed by the addition of mevalonic acid. Thus, both normal and transformed cells require mevalonate, or an as yet unidentified metabolite of mevalonate for their growth, even though some transformed cells have become relatively autonomous of other growth factors. Whereas mevinolin acted primarily as a cytostatic agent for most of the cell lines studied, with the transformed cell line MCA/10T 1/2, which ordinarily grows to a very high cell density, prolonged exposure to mevinolin caused marked cytotoxicity. Thus mevinolin might be useful as an anti-tumor agent for specific tumors.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041270205
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  • 8
    Electronic Resource
    Electronic Resource
    Membrane effects of tumor promoters: Stimulation of sugar uptake in mammalian cell cultures (1979)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 99 (1979), S. 451-460 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Phorbol esters stimulate 2-deoxy-D-glucose (DG) uptake in rodent and human cell cultures. The potent tumor promoting agent, 12-0-tetradecanoyl phorbol-13 acetate (TPA), induces a 12-fold stimulation in confluent 3T3 cells and a 2.5-fold stimulation in HeLa cells. When a series of macrocyclic diterpenes are assayed, their relative potencies in stimulating DG uptake in 3T3 cells correlate with other known biologic effects of these compounds. On a molar basis, TPA is a much more potent stimulator of DG transport than insulin or epidermal growth factor. In HeLa cells, the ED50 value of the TPA effect is 0.2 nM. The increase in DG uptake occurs immediately after the addition of TPA, reaches a maximum at 90 minutes, persists for at least three hours after removal of TPA from the medium, and is temperature dependent. The stimulation is not inhibited by cycloheximide or actinomycin D. As in control cells, DG uptake in TPA treated cells is inhibited by p-hydroxymercuribenzoate, phloridzin, cytochalasin B, and dexamethasone. Although the precise mechanism is not known, evidence is presented that the TPA stimulation of DG uptake is due to enhanced transport of the sugar rather than to effects of intracellular metabolism. The enhanced transport may be secondary to a more generalized change in membrane structure.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1040990319
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  • 9
    Electronic Resource
    Electronic Resource
    Control of melanin synthesis and secretion by B16/C3 melanoma cells (1982)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 113 (1982), S. 481-486 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: In culture, B16/C3 murine melanoma cells grown in the presence of serum undergo melanogenesis at a specific time after plating. At this time, melanin is synthesized intracellularly and then secreted into the extracellular culture fluid. We have found that melanin secretion is dependent on the presence of serum in the growth medium. When confluent cultures are deprived of serum, that is, refed with serum-free medium, cells remain viable but do not undergo melanogenesis. Addition of serum-free medium supplemented with either melanocyte-stimulating hormone (MSH) or dibutyryl cAMP induced melanogenesis in these cells but did not result in melanin secretion. Furthermore, when B16/C3 cells are grown in serum-free, hormone-supplemented medium, they also undergo melanogenesis but fail to release melanin. The addition of serum, however, to B16/C3 cells induced to undergo melanogenesis with MSH, dibutyryl cAMP, or hormone-supplemented medium promotes melanin secretion. Fractionation studies hence revealed that serum contains specific factors capable of inducing melanin secretion. These results demonstrate that factors that regulate melanin synthesis are distinct from those that induce cells to release melanin into their extracellular environment. Furthermore, the ability to induce melanogenesis with single factors will permit us to study the precise sequence of events leading to differentiation in B16/C3 cells under chemically defined conditions.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041130318
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  • 10
    Electronic Resource
    Electronic Resource
    Amphiphilic cationic peptides mediate cell adhesion to plastic surfaces (1985)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 124 (1985), S. 365-371 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Four amphiphilic peptides, each with net charges of +2 or more at neutrality and molecular weights under 4 kilodaltons, were found to mediate the adhesion of normal rat kidney fibroblasts to polystyrene surfaces. Two of these peptides, a model for calcitonin (peptide 1, MCT) and melittin (peptide 2, MEL), form amphiphilic α-helical structures at aqueous/nonpolar interfaces. The other two, a luteinizing hormone-releasing hormone model (peptide 3, LHM) and a platelet factor model (peptide 4, MPF) form β-strand structures in amphiphilic environments. Although it contains only 10 residues, LHM mediated adhesion to surfaces coated with solutions containing as little as 10 pmoles/ml of peptide. All four of these peptides were capable of forming monolayers at air-buffer interfaces with collapse pressures greater than 20 dynes/cm. None of these four peptides contains the tetrapeptide sequence Arg-Gly-Asp-Ser, which has been associated with fibronectin-mediated cell adhesion. Ten polypeptides that also lacked the sequence Arg-Gly-Asp-Ser but were nonamphiphilic and/or had net charges less than +2 at neutrality were all incapable of mediating cell adhesion (Pierschbacher and Ruoslahti, 1984). The morphologies of NRK cells spread on polystyrene coated with peptide LHM resemble the morphologies on fibronectin-coated surfaces, whereas cells spread on surfaces coated with MCT or MEL exhibit strikingly different morphologies. The adhesiveness of MCT, MEL, LHM, and MPF implies that many amphiphilic cationic peptides could prove useful as well defined adhesive substrata for cell culture and for studies of the mechanism of cell adhesion.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041240302
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