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  • 1
    Electronic Resource
    Electronic Resource
    Colocalization of the p185HER2 oncoprotein and integrin α6β4 in Calu-3 lung carcinoma cells (1994)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 55 (1994), S. 409-418 
    Details
    ISSN: 0730-2312
    Keywords: HER2/neu ; integrins ; laminin ; tyrosine phosphorylation ; oncoprotein ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Anti-p185HER2 monoclonal antibodies often show intense reactivity with the basement membrane of tumor cells that overexpress the HER2/neu gene product (p185HER2). To evaluate a possible interaction between p185HER2 and adhesion molecules or their receptors, the polarity of p185HER2 was tested in lung carcinoma cell line Calu-3, which overexpresses this protein, in cultures grown as confluent monolayers or as aggregates. MAb immunostaining patterns indicated that p185HER2 is concentrated on the baso-lateral membrane of cells and that it colocalizes with the integrin α6β4 at the cell-cell junctions where laminin is also found. The same membrane region showed intense reactivity with antiphosphotyrosine antibodies. Furthermore, integrin clustering induced by the specific antibody was accompanied by the clustering of p185HER2, as indicated by immunoelectron microscopy, and by a subsequent increase in p185HER2 tyrosine phosphorylation. Treatment with exogenous laminin also resulted in increased basal levels of p185HER2 phosphorylation. These data suggest a physical interaction between the integrin and the oncoprotein that might be functionally relevant in directly controlling the tyrosine phosphorylation of the catalytic domain of p185HER2. © 1994 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240550402
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  • 2
    Electronic Resource
    Electronic Resource
    Genetic changes in lung cancer (1993)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 53 (1993), S. 237-248 
    Details
    ISSN: 0730-2312
    Keywords: cytogenetics ; oncogenes ; tumor suppressor genes ; growth factor receptors ; normal epithelium ; lung cancer ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: In an attempt to define the type and temporal sequences of somatic genetic changes that precede the onset of invasive lung cancer, and to search for biological markers useful in screening multiple primary tumors of the upper aerodigestive tract, we have performed a cytogenetic and genetic study using normal bronchial epithelium and primary tumor specimens of 68 patients undergoing pulmonary resection for early stage lung cancer, and normal bronchial epithelium of 5 controls with metastatic sarcomas. Of the 68 lung cancer cases, 31 had a single tumor and 37 displayed multiple synchronous or metachronous tumors. Cytogenetic alterations were observed in 59% (23/39) of the evaluable tumor specimens with complex rearranged karyotypes, particularly involving chromosomes 3 (70%), 17 (39%), 11 (26%), 8, 9, 12 (22%), and 7 (17%). Gene alterations were also detected including overexpression of epidermal growth factor receptor (EGFR) in 63% (36/57), HER2/NEU in 21% (12/56), and p53 mutations in 50% (12/24). The overall frequency of genetic changes (any type) in the tumors was 76% (52/68). In the normal bronchial mucosa, we identified a rearranged karyotype in 20% of the evaluable cases (13/63); particularly simple rearrangements involving chromosomes 3p (6 cases), 7 (6 cases), 17 (3 cases), 9, 11 (2 cases), 8 (1 case); as well as overexpression of EGFR in 39% (20/51) and of HER2/NEU in 14% (7/51). The overall frequency of genetic changes (any type) in the normal epithelium was 46% (30/65). The presence of a rearranged karyotype in the bronchial mucosa was associated with a rearranged karyotype in the tumor sample. Other statistically significant correlations were found between histopathologic and clinical features and the occurrence of the different cytogenetic and genetic changes both in tumors and in the normal bronchial mucosa. No genetic abnormalities were found in the bronchial epithelium of the 5 controls.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcb.240531035
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  • 3
    Electronic Resource
    Electronic Resource
    Formation of the 67-kDa laminin receptor by acylation of the precursor (1998)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 69 (1998), S. 244-251 
    Details
    ISSN: 0730-2312
    Keywords: monomeric laminin receptor ; receptor maturation ; acylation ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Even though the involvement of the 67-kDa laminin receptor (67LR) in tumor invasiveness has been clearly demonstrated, its molecular structure remains an open problem, since only a full-length gene encoding a 37-kDa precursor protein (37LRP) has been isolated so far. A pool of recently obtained monoclonal antibodies directed against the recombinant 37LRP molecule was used to investigate the processing that leads to the formation of the 67-kDa molecule. In soluble extracts of A431 human carcinoma cells, these reagents recognize the precursor molecule as well as the mature 67LR and a 120-kDa molecule. The recovery of these proteins was found to be strikingly dependent upon the cell solubilization conditions: the 67LR is soluble in NP-40-lysis buffer whereas the 37LRP is NP-40-insoluble. Inhibition of 67LR formation by cerulenin indicates that acylation is involved in the processing of the receptor. It is likely a palmitoylation process, as indicated by sensitivity of NP-40-soluble extracts to hydroxylamine treatment. Immunoblotting assays performed with a polyclonal serum directed against galectin3 showed that both the 67- and the 120-kDa proteins carry galectin3 epitopes whereas the 37LRP does not. These data suggest that the 67LR is a heterodimer stabilized by strong intramolecular hydrophobic interactions, carried by fatty acids bound to the 37LRP and to a galectin3 cross-reacting molecule. J. Cell. Biochem. 69:244-251, 1998. © 1998 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Shedding of the 67-kD laminin receptor by human cancer cells (1996)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 60 (1996), S. 226-234 
    Details
    ISSN: 0730-2312
    Keywords: monomeric laminin receptor ; shedding ; metastasis ; double determinant assay ; adhesion ; prognostic factor ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The 67-kD laminin receptor (67LR) is a cell membrane-associated molecule exhibiting high affinity for the basement membrane glycoprotein, laminin. While export of the 67LR toward the extracellular matrix has been recently suggested by electron microscopy studies, there is to date no evidence of shedding of the 67LR from cells. Using two monoclonal antibodies directed against the 67LR, we developed a double-determinant radioimmunoassay that demonstrates that the 67LR is released from cancer cells into the culture medium. The shed molecule exhibited the same apparent molecular weight as that of the membrane-associated 67LR, suggesting that no proteolytic cleavage is involved in the process. Furthermore, we demonstrate that the 67LR is not anchored to the membrane through a glycolsyl-phosphatidylinositol bridge. However, the observation that lactose increased the release of 67LR suggests that a lectin-type interaction is involved in the cell membrane association of this laminin binding protein and the cell surface. Interestingly, the released 67LR recovered after HPLC gel filtration was found free as well as associated to high molecular weight complexes. The free 67LR retained its ability to bind to the cell surface. Our study is the first demonstration that the 67LR is effectively shed by cancer cells. The released free 67LR could play an important role in modulating interactions between cancer cells and laminin during tumor invasion and metastasis. © 1996 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
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  • 5
    Electronic Resource
    Electronic Resource
    New insights into the metastasis-associated 67 kD laminin receptor (1997)
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 67 (1997), S. 155-165 
    Details
    ISSN: 0730-2312
    Keywords: adhesion receptors ; tumor progression ; ribosomal proteins ; laminin ; cancer ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: The interactions between tumor cells and laminin or other components of the extracellular matrix have been shown to play an important role in tumor invasion and metastasis. These interactions are mediated by different cell surface molecules, including the monomeric 67 kD laminin receptor. This molecule appears to be very peculiar since so far only a full-length gene encoding a 37 kD precursor protein has been isolated and the mechanism by which the precursor reaches the mature form is not understood. Based on clinical data, which clearly demonstrate the importance of the receptor in tumor progression, studies were conducted to define the structure, expression, and function of this laminin receptor as a step toward developing therapeutic strategies that target this molecule. The data suggest that acylation of the precursor is the key mechanism in maturation of the 67 kD form. The function of the membrane receptor is to stabilize the binding of laminin to cell surface integrins, acting as an integrin-accessory molecule, although homology of the gene encoding the receptor precursor with other genes suggests additional functions. Downregulation of the receptor expression on tumor cells might open new therapeutic approaches to decrease tumor aggressiveness. J. Cell. Biochem. 67:155-165, 1997. © 1997 Wiley-Liss, Inc.
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  • 6
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    Author Correction: The landscape of d16HER2 splice variant expression across HER2-positive cancers (2020)
    Springer Nature
    Details
    Publication Date: 2020-04-24
    Electronic ISSN: 2045-2322
    Topics: Natural Sciences in General
    Published by Springer Nature
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  • 7
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    The lung microbiota: role in maintaining pulmonary immune homeostasis and its implications in cancer development and therapy (2020)
    Springer
    Details
    Publication Date: 2020-01-23
    Print ISSN: 1420-682X
    Electronic ISSN: 1420-9071
    Topics: Biology , Medicine
    Published by Springer
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  • 8
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    cIAP1 regulates the EGFR/Snai2 axis in triple-negative breast cancer cells (2018)
    Springer Nature
    Details
    Publication Date: 2018-04-19
    Print ISSN: 1350-9047
    Electronic ISSN: 1476-5403
    Topics: Biology , Medicine
    Published by Springer Nature
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  • 9
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    TLR3 Expression Induces Apoptosis in Human Non-Small-Cell Lung Cancer (2020)
    Molecular Diversity Preservation International
    Details
    Publication Date: 2020-02-20
    Description: The prognostic value of Toll-like receptor 3 (TLR3) is debated in cancer, differing between tumor types, methods, and cell types. We recently showed for the first time that TLR3 expression on early stage non-small-cell lung cancer (NSCLC) results associated with a good prognosis. Here, we provide experimental evidences explaining the molecular reason behind TLR3’s favorable prognostic role. We demonstrated that TLR3 activation in vitro induces apoptosis in lung cancer cell lines and, accordingly, that TLR3 expression is associated with caspase-3 activation in adenocarcinoma NSCLC specimens, both evaluated by immunohistochemistry. Moreover, we showed that TLR3 expression on cancer cells contributes to activate the CD103+ lung dendritic cell subset, that is specifically associated with processing of antigens derived from apoptotic cells and their presentation to CD8+ T lymphocytes. These findings point to the relevant role of TLR3 expression on lung cancer cells and support the use of TLR3 agonists in NSCLC patients to re-activate local innate immune response.
    Print ISSN: 1661-6596
    Electronic ISSN: 1422-0067
    Topics: Chemistry and Pharmacology
    Published by Molecular Diversity Preservation International
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  • 10
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    Cytotoxic Activity of Histone Deacetylase Inhibitor ITF2357 on Burkitt’s Lymphoma Cell Lines Is Associated to Micro-RNA Modulation and Transglutaminase 2 Restoration. (2008)
    American Society of Hematology
    Details
    Publication Date: 2008-11-16
    Description: Background and Objectives: The significant toxicities associated with current treatments of Burkitt’s lymphoma (BL) have fostered the identification of novel targets for effective but less toxic therapies. c-myc overexpression is the hallmark of BL; however it is per se insufficient to cause lymphoma development. Recent studies indicating aberrant expression of microRNAs (miRNAs) in BL have raised the possibility of a c-myc - miRNA interaction within the genesis and the maintenance of the lymphoma phenotype. Myc oncoproteins indeed have been found to inhibit the transcription of tumor suppressor genes. This occurs for instance by recruiting histone deacetylase (HDAC) 1 proteins to target genes, including tissue transglutaminase 2 (TG2), a multifunctional protein that promotes apoptosis and differentiation in normal tissues. Since inhibitors of the epigenetic regulator HDACs are revealing very effective as anticancer agents, we evaluated ITF2357, a new hydroxamate inhibitor of HDAC, with respect to its ability to induce proliferative arrest and apoptosis in BL cell lines by modulating c-myc mRNA, miRNAs and TG2 expression. Methods and Results: Cell growth inhibition by ITF2357 was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay in the BL cell lines Namalwa and Raji. ITF2357 IC50 was 200nM after 48h exposure. Most treated Namalwa and Raji cells became respectively late and early apoptotic as assessed by annexin V and propidium iodide staining. Accordingly, ITF235 induced SUBG1 peak formation in Namalwa cells and G1 arrest in Raji cells. Repeated addition of ITF2357 at 24h-intervals enhanced these effects. Array analyses and quantitative real-time PCR of miRNAs indicated a significant decrease in the expression of miR-155 and miR-98, which exert oncogenic activity in MYC-associated tumors, at 24–72 h after treatment. Conversely, the Let-7a miRNA, which targets the c-MYC mRNA stabilizer IMP-1 among its tumor suppressive functions, was up regulated peaking at 24h after drug administration. Finally, immunohistochemical analysis of TG2 expression in ITF2357-treated Raji cells revealed a diffuse cytoplasmic staining, whereas in their untreated counterparts TG2 was sporadically and faintly detectable. Despite ITF2357 restored the expression of different targets of myc, quantitative real-time PCR revealed no parallel decrease in c-myc mRNA suggesting that the epigenetic modulation provided by ITF2357 on BL cell lines did not directly affect myc expression level. Conclusion: Our data indicate potent cytotoxic and growth inhibitory activities of ITF2357 on BL cell lines. These effects might be related to the modulation of both oncogenic and tumor-suppressing miRNAs and to the restoration of the tumor suppressor TG2. Further evidences for the potential candidacy of ITF2357 as a therapeutic agent for BL awaits ongoing analyses in BL primary tumors and in animal models.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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