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  • 1
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1520-4804
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] B16 clones were isolated and cultured in vitro as described previously6-8. Challenge with MSH or forskolin and measurement of cellular cyclic AMP was performed as described in Table 1 legend. MSH binds to specific cell-surface receptors that are coupled via a regulatory protein(s) to adenylate ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 282 (1979), S. 738-739 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Our cell aggregation assay is based on the fact that if a fluid or cell suspension is subjected to a constant rate of shear in a viscometer, the shear stress (force per unit area) generated at the measuring element of the apparatus is proportional to the rate at which energy is dissipated ...
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 488 (1986), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1573-7276
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of DNA methylation in the generation of tumor cell variants with altered growth behavior has been investigated. Cultures of the clonally heterogeneous B16 melanoma cell line and a clonal population (B16-CL) derived from it were treated with the DNA hypomethylating agent, 5-azacytidine (5-Aza-CR). The tumorigenic and metastatic properties of (sub)clones isolated from these cultures before and after drug treatment were assayed by injection via multiple routes into syngeneic C57BL/6 mice using a range of cell doses. The rate of tumor growth was monitored following intrafootpad (i.f.p.) injection and the tumor incidence was calculated from the frequency of tumor formation at i.f.p. and supraclavicular subcutaneous (s.c.) sites. Formation of both spontaneous (i.f.p., s.c. inoculations) and experimental (intravenous (i.v.) inoculation) metastatic potential was also investigated. The most consistent effect of 5-Aza-CR was the introduction of heterogeneity with respect to the tumorigenic phenotype. The effect of 5-Aza-CR treatment on metastatic behavior was variable. The majority of tumor cell variants that arose following 5-Aza-CR treatment displayed decreased malignant potential and reduced DNA methylation levels relative to untreated control cells, but the correlation was not absolute. The decreases in DNA methylation levels induced by 5-Aza-CR were unstable and began to rebound within 1 week of drug treatment. The results of the current study indicate that although 5-Aza-CR can introduce significant shifts in the malignant properties of treated cells, the direction and magnitude of the induced alterations are not predictable and are influenced by a variety of experimental parameters including the starting tumor cell population, route of tumor cell inoculation, and the drug treatment protocol. In addition, because DNA methylation levels can rebound rapidly (days) it is difficult to correlate changes in this parameter with the observed alterations in malignancy, which can only be assessed in long-term biological assays (weeks).
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Cancer and metastasis reviews 5 (1986), S. 3-14 
    ISSN: 1573-7233
    Keywords: chemotherapy ; growth regulation ; paracrine ; predisposition factors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The eradication of established metastases in patients with malignant tumors is the single most important objective in clinical oncology. The current panel of antineoplastic agents discovered through random and semiempirical screening procedures has proven largely ineffective in treating disseminated disease and there is a clear and urgent need for more efficient antimetastatic drugs. Unfortunately, although progress has been made in examining the biology of metastatic spread, our understanding of the pharmacology, biochemistry and molecular genetics of this process is meager and insufficient to provide a rational foundation for the design of mechanism-based antineoplastic agents. Faced on the one hand with the failure of existing drugs to control metastatic spread and on the other with a dearth of alternative pharmacological approaches, the prospect of offering significantly improved therapy to the cancer patient of the 1990's is poor. The challenge of the coming decade lies in obtaining better insights into the molecular mechanisms of metastasis and using this information to identify pharmacological opportunities to curtail the proliferation of secondary tumor growths. As a first step toward this goal we need to define more rigorously what constitutes a therapeutic target in malignant disease and what steps in the pathogenesis of cancer metastasis represent the gravest risk to the patient and thus are most eligible for direct pharmacological intervention. In addressing these issues and developing future strategies for antimetastatic drugs, Paget's 100 year-old ‘seed and soil’ hypothesis continues to offer a useful conceptual framework for analysis of metastatic behavior. Although Paget's proposal has been validated by a century of clinical observation, efforts to define the ‘seed and soil’ theory in molecular terms have not been attempted. With the advent of more efficient methodologies for culturing human normal and neoplastic cells coupled with the availability of microanalytical technologies it now becomes possible to investigate and identify the complementary biochemical components of the tumor cell ‘seed’ and organ ‘soil’ that combine to encourage the proliferation of metastases. With this information the design of specific pharmacological strategies to uncouple the ‘seed and soil’ relationship may emerge as a potential therapeutic approach for antagonizing the growth of disseminated malignant tumors.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 44 (1990), S. 229-239 
    ISSN: 0730-2312
    Keywords: adrenocortical carcinoma cells ; protein purification ; anchorage independent growth ; epithelial cell proliferation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: A polypeptide growth factor has been partially purified from medium conditioned by the human adrenocortical carcinoma cell line SW13. This factor, designated h-TGFe, stimulates anchorage-independent growth of the SW13 cells. Similar activity was observed in human milk, and in conditioned media from seven of 14 epithelial cell lines. The SW13-derived activity is stable to low pH and 8M urea but labile to dithiothreitol and 2% sodium dodecyl sulfate. Human TGFe does not bind to heparin and fails to stimulate growth of endothelial cells in monolayer culture. The apparent molecular weight of h-TGFe is 59k by size exclusion chromatography in the presence of 8M urea and the activity binds strongly to cation exchangers. The activity elutes at 15-30% acetonitrile from a C18 reversephase column and has been partially purified by using a four-step chromatographic procedure. TGFe appears to be a novel growth factor produced by many epithelial cells and tissues.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
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