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  • 1
    Electronic Resource
    Electronic Resource
    Radiotherapy for genes that cause cancer (1995)
    [s.l.] : Nature Publishing Group
    Nature medicine 1 (1995), S. 1215-1217 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Conventional radiotherapy for cancer achieves a therapeutic advantage by exploiting differences between tumour and normal tissue with respect to repair, cell-cycle redistribution, repopulation, and reoxygenation, and by limiting the dose received by critical normal tissues. The probability of ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm1195-1215
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  • 2
    Electronic Resource
    Electronic Resource
    To metastasize or not? Selection of CD44 splice sites (1995)
    [s.l.] : Nature Publishing Group
    Nature medicine 1 (1995), S. 635-637 
    Details
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Following the initial demonstration by Gunthert et al.1 that a variant of the widely distributed cell surface adhesion protein CD44 could confer metastatic potential on a rat pancreatic adenocarcinoma cell line, a great deal of scientific interest has focused on attempting to better define the role ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nm0795-635
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  • 3
    Electronic Resource
    Electronic Resource
    Inhibitory effect of locally produced and exogenous interleukin-6 on tumor growth in vivo (1994)
    Springer
    Cancer immunology immunotherapy 38 (1994), S. 339-345 
    Details
    ISSN: 1432-0851
    Keywords: Interleukin-6 ; Tumor-associated macrophages ; Gene therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to define the potential antitumor activity of the multifunctional cytokine interleukin-6 (IL-6), retrovirus-mediated gene transfer was used to introduce and express a cDNA encoding human IL-6 in the murine fibrosarcoma cell line Fsa-R. Although these genetically modified tumor cells appeared morphologically and phenotypically identical to control Fsa-R cells and had a similar plating efficiency in vitro, they were found to exhibit greatly reduced tumorigenicity in vivo following intravenous injection into syngeneic recipients. Exogenous IL-6 was shown to produce a similar inhibition of tumor growth in the lung if administered intraperitoneally. In contrast, tumor growth in subcutaneous sites was inhibited only if the tumor cells were engineered to express IL-6 locally, or if IL-6 was administered intratumorally. Intraperitoneal injection of IL-6 had no inhibitory effect. Tumors that did grow from IL-6-producing tumor cell inocula in subcutaneous sites were found to contain large numbers of macrophages. These results demonstrate that the antitumor activity of systemically administered IL-6 varies depending on the site of tumor growth and suggest an important role for IL-6 in the recruitment, proliferation and/or survival of tumor-associated macrophages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01525513
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  • 4
    Electronic Resource
    Electronic Resource
    Immunoregulating activity of tumor-associated macrophages (1986)
    Springer
    Cancer immunology immunotherapy 23 (1986), S. 67-72 
    Details
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In this report, we examine the antigen nonspecific immunoregulating activity of macrophages isolated from the murine methylcholanthrene-induced fibrosarcoma FSA. These cells were shown to enhance the primary anti-CRBC PFC response of whole normal spleen cells in a dose-dependent fashion. This function was associated with a subpopulation of large Ia-negative macrophages and was mediated by a soluble macrophage-derived factor that appeared to act by stimulating the proliferation and/or differentiation of antigen-reactive T cells. The relationship of this factor to previously described monokines is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00205558
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  • 5
    Electronic Resource
    Electronic Resource
    Inhibitory effect of locally produced and exogenous interleukin-6 on tumor growth in vivo (1994)
    Springer
    Cancer immunology immunotherapy 38 (1994), S. 339-345 
    Details
    ISSN: 1432-0851
    Keywords: Key words: Interleukin-6 – Tumor-associated macrophages – Gene therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. In order to define the potential antitumor activity of the multifunctional cytokine interleukin-6 (IL-6), retrovirus-mediated gene transfer was used to introduce and express a cDNA encoding human IL-6 in the murine fibrosarcoma cell line Fsa-R. Although these genetically modified tumor cells appeared morphologically and phenotypically identical to control Fsa-R cells and had a similar plating efficiency in vitro, they were found to exhibit greatly reduced tumorigenicity in vivo following intravenous injection into syngeneic recipients. Exogenous IL-6 was shown to produce a similar inhibition of tumor growth in the lung if administered intraperitoneally. In contrast, tumor growth in subcutaneous sites was inhibited only if the tumor cells were engineered to express IL-6 locally, or if IL-6 was administered intratumorally. Intraperitoneal injection of IL-6 had no inhibitory effect. Tumors that did grow from IL-6-producing tumor cell inocula in subcutaneous sites were found to contain large numbers of macrophages. These results demonstrate that the antitumor activity of systemically administered IL-6 varies depending on the site of tumor growth and suggest an important role for IL-6 in the recruitment, proliferation and/or survival of tumor-associated macrophages.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01525513
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Role of macrophage-colony-stimulating factor in regulating the accumulation and phenotype of tumor-associated macrophages (1997)
    Springer
    Cancer immunology immunotherapy 44 (1997), S. 165-172 
    Details
    ISSN: 1432-0851
    Keywords: Key words Tumor-associated macrophages ; M-CSF ; op/op mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In order to better define the role played by tumor-cell-derived macrophage-colony-stimulating factor (M-CSF) in regulating the recruitment and phenotype of tumor-associated macrophages, Polyoma large T-transformed fibroblastoid cell lines, derived from M-CSF-deficient osteopetrotic op/op mice and their phenotypically normal op/+ littermate controls, were inoculated into SCID (severe combined immunodeficiency) recipients and both the proportion and phenotype of the macrophages present within the tumors generated were determined. The results obtained indicate that, although tumors derived from M-CSF-deficient and M-CSF-producing tumor cell inoculate contain a similar proportion of macrophages, the macrophages isolated from tumors lacking M-CSF appear morphologically less mature and express lower levels of interleukin 1β, tumor necrosis factor α and FcRγII mRNA. Taken together, these data suggest that, although M-CSF does not appear to play a critical role in determining the macrophage content of these tumors, it does play a role in modulating the phenotype, and potentially the functional activity of the macrophages present within the tumor microenvironment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002620050369
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  • 7
    Electronic Resource
    Electronic Resource
    Newly discovered anti-inflammatory properties of the benzamides and nicotinamides (1999)
    Springer
    Molecular and cellular biochemistry 193 (1999), S. 119-125 
    Details
    ISSN: 1573-4919
    Keywords: benzamides ; nicotinamides ; apoptosis ; inflammation ; NF-kB ; DNA repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Our laboratory has concentrated on the possible regulation the benzamides and nicotinamides may have on the processes of DNA repair and apoptosis. Recent reports [14-16] have suggested that both apoptosis and inflammation are regulated by the transcription factor NF-kB. We have initiated studies regarding the hypothesis that the benzamides and nicotinamides could inhibit the production of tumor necrosis factor alpha (TNFalpha) and the inflammatory response as well as induce apoptosis via inhibition of NF-kB. Our data have shown that nicotinamide and two N-substituted benzamides, metoclopramide (MCA) and 3-chloroprocainamide (3-CPA), gave dose dependent inhibition of lipopolysacharide induced TNFalpha in the mouse within the dose range of 10-500 mg/kg. Moreover, lung edema was prevented in the rat by 3 ï 50 mg/kg doses of 3-CPA or MCA, and 100-200 μM doses of MCA could also inhibit NF-kB in Hela cells. Taken together these data strongly support the notion that benzamides and nicotinamides have potent anti-inflammatory and antitumor properties, because their primary mechanism of action is regulated by inhibition at the gene transcription level of NF-kB, which in turn inhibits TNFalpha and induces apoptosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006932714982
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  • 8
    Electronic Resource
    Electronic Resource
    Gene therapeutic approach to primary and metastatic brain tumors: I. CD44 variant pre-RNA alternative splicing as a CEPT control element (1995)
    Springer
    Journal of neuro-oncology 26 (1995), S. 243-250 
    Details
    ISSN: 1573-7373
    Keywords: CD44 ; VDEPT ; CEPT ; alternative splicing ; gene targeting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Our laboratory and others have shown alternative splicing of up to ten exons at a discrete extracellular site to be primarily responsible for the generation of CD44 variant (CD44v) isoforms. Based on clear differences in the expression of these CD44v isoforms between normal and malignant tissues, we believe that elucidation of the mechanisms underlying the regulation of CD44 alternative splicing may provide a new gene therapeutic targeting approach based on CD44 pre-mRNA processingin vivo. This strategy incorporates utilization of CD44 alternative splicing control elements into a chimeric enzyme/prodrug therapy (CEPT), a novel modification of the virus-directed enzyme/prodrug therapy (VDEPT) approach for the treatment of brain metastases from tumors of systemic origin. As initial steps towards the development of a gene therapeutic approach based on targeting tumor cell expression of specific CD44v alternatively spliced isoforms, we have: (1) developed a novelin vivo assay system that allows the rapid analyses of potentially therapeutic CD44 alternative splicing minigene constructs; and (2) cloned theE. coli cytosine deaminase (CD) gene and fused its enzymatically active domain to alternatively spliced CD44 exons (CD44/CD). Deamination of cytosine by this CD44/CD chimeric fusion protein is demonstrated inE. coli cell lysates to be equal to that of wild type cytosine deaminase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01052627
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  • 9
    Electronic Resource
    Electronic Resource
    Molecular mechanisms regulating the hyaluronan binding activity of the adhesion protein CD44 (1995)
    Springer
    Journal of neuro-oncology 26 (1995), S. 231-239 
    Details
    ISSN: 1573-7373
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In the present study, we describe the isolation and characterization of a cDNA clone designated B6F1.3, that appears to ‘activate’ the hyaluronan-binding capacity of CD44 upon transfection into the murine fibroblastoid cell line MOP8. Sequence analysis indicates that the putative regulatory molecule encoded by this clone is identical to the murine interleukin-2 receptor γ chain (mIL-2Rγ), a recently described type 1 transmembrane protein that constitutes an integral component of the cell surface receptors that bind a number of cytokines including IL-2, IL-4, IL-7, IL-9, IL-15 and perhaps also IL-13. Mutations in this molecule have been shown to be responsible for X-linked severe combined immunodeficiency (XSCID) in humans. With the exception of bone marrow, the mIL-2Rγ chain was found to be expressed at high levels on all hemopoietic cell lines and tissue types examined. Non-hemopoietic tissues are generally negative. FACS analysis and Western blot analysis indicated respectively that B6F1.3 does not mediate its effects by upregulating the expression of CD44 or by altering the alternative splicing of the molecule. Removal of the cytoplasmic tail of the mIL-2Rγ chain, including a Src homology region 2 (SH2) subdomain, abolished its ability to enhance CD44-mediated binding to hyaluronan suggesting the involvement of signal transduction events triggered via the cytoplasmic domain in the ‘activation’ process. Determining whether activating molecules such as B6F1.3 are co-expressed within tumor cells may help improve the potential value of CD44 as a diagnostic marker of metastatic disease.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01052626
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  • 10
    Electronic Resource
    Electronic Resource
    Preface (1995)
    Springer
    Journal of neuro-oncology 26 (1995), S. 161-161 
    Details
    ISSN: 1573-7373
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01052618
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