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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Biotechnology letters 22 (2000), S. 1553-1556 
    ISSN: 1573-6776
    Keywords: fibroblast cell ; gel ; GRGDS ; integrin family ; N-isopropylacrylamide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract High molecular weight N-isopropylacrylamide copolymers with small amounts of acrylic acid (typically 2–5 mol% in feed) were synthesized by free radical polymerization in benzene and then conjugated with adhesion molecules of Gly-Arg-Gly-Asp-Ser (GRGDS) peptides. Aqueous polymer solutions (5, 6, 8 and 10% w/v) in culture medium (pH 7.4, ionic strength; 0.15 M) with 3T3-L1 fibroblast cells were mixed and poured in Millicells, which supported the gel formation without a significant gel induction time at 36 °C (gelation temperature). The initially formed gel was translucent and became more opaque as the temperature increased. The interaction between fibroblast cells and an artificial matrix of GRGDS containing p(NiPAAm-co-AAc) copolymer gel resulted in effective cell attachment, proliferation and growth. This study supported that specific attachment is the result of the interaction between the integrin families on the fibroblast and the RGD sequence on the p(NiPAAm-co-AAc) copolymer gel.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0219-1032
    Keywords: DNA Methylation ; Head and Neck Squamous Cell Carcinoma ; p16INK4a
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Inactivation of the p16INK4a gene by mutation and deletion is common in head and neck squamous cell carcinoma (HNSCC). The present study demonstrates that hypermethylation of the 5′ CpG islands can serve as an alternative mechanism for the inactivation of the p16INK4a gene in this tumor. We studied 11 HNSCC cell lines and 17 oral squamous cell carcinoma (OSCC) primary tumors for p16INK4a gene status by protein/mRNA and DNA genetic/epigenetic analyses to determine the incidence of its inactivation. Our study indicates that: (1) inactivation of p16 protein is frequent in HNSCC cell lines (6/11, 54.5%) and OSCC primary tumors (15/17, 88.2%), (2) inactivation of p16INK4a protein is commonly associated with the presence of gene alteration such as mutation, homozygous deletion and especially aberrant methylation, and (3) genomic sequencing of bisulfite-modified DNA shows that the carcinoma develops a heterogeneous pattern of hypermethylation.
    Type of Medium: Electronic Resource
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