In vitro and in vivo regulation of tumor antigen expression by human recombinant interferons |
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Affiliation: | 1. Graduate Institute of Pharmacognosy, Taipei Medical University, 252 Wu Hsing Street, Taipei 110, Taiwan;2. Division of Hog Cholera Research, Animal Health Research Institute, Council of Agriculture, 376 Chung-Cheng Road, New Taipei City 251, Taiwan;3. School of Pharmacy, China Medical University, 91 Hsueh-Shih Road, Taichung 404, Taiwan;4. Department of Biomedical and Environmental Biology, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan;5. Institute of Bioinformatics and Biosignal Transduction, College of Bioscience and Biotechnology, National Cheng Kung University, 1 University Road, Tainan 701, Taiwan;6. Graduate Institute of Medicine, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan;7. Center for Biomarkers and Biotech Drugs, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan |
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Abstract: | In vitro treatment with either type I or type II Interferon (IFN) can selectively enhance the expession of several tumor antigens, such as the carcinoembryonic antigen (CEA) and the tumor-associated glycoprotein-72 (TAG-72) in different human carcinoma cell lines and result in enhanced level of monoclonal antibody (MAb) binding to the cell surface. In vivo animal studies demonstrated that treatment of athymic mice with a type I interferon [i.e. interferon-α(A)]significantly increased the expression of a 90 kDa tumor antigen which improved the targeting of a MAb to the carcinoma xenograft. More recent studies reported that in vitro IFN treatment of human adenocarcinoma cells isolated from human malignant serous effusions selectively increased the expression of TAG-72 and CEA. One can envision that the ability of these cytokines to upregulate the level of expression of human tumor antigens presents an important experimental model in which to study the regulation of markers often correlated with epithelial cell differentiation. In addition, the increase of selective MAb-defined antigens may also be exploited in an adjuvant setting to localize higher amounts of MAbs to the tumor cell surface and, thereby, improve the effectiveness of a MAb for tumor diagnosis and, possibly, therapy. |
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