Abstract
Metastatic clones of murine tumors that manifest impaired expression of class I MHC antigens do not induce an antitumor CTL activity. Transfection of H-2Kb genes into D122 carcinoma and B16 melanoma clones converted these cells to low metastatic immunogenic clones that can be used to protect in vivo against metastases of parental clones. Amplification of the protective effect can be achieved by combination of syngeneic and allogeneic MHC class I genes. Studying the mechanisms involved in MHC class I suppression in tumor cells, we found that changes in H-2 promoter activity were the cause of low expression. Proteins that might be involved were demonstrated by migration retardation methods. The involvement of the fos-jun complex in regulation of MHC expression is discussed.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Antigens, Neoplasm / genetics
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Antigens, Neoplasm / immunology*
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Base Sequence
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Gene Expression Regulation, Neoplastic
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Genes, MHC Class I*
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H-2 Antigens / genetics
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H-2 Antigens / immunology*
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Major Histocompatibility Complex
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Mice
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Molecular Sequence Data
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Neoplasm Metastasis / genetics*
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Neoplasm Metastasis / immunology
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Neoplasm Proteins / biosynthesis
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Neoplasm Proteins / genetics
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Neoplasm Transplantation
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Neoplasms, Experimental / genetics
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Neoplasms, Experimental / immunology
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Neoplasms, Experimental / pathology
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Oncogenes
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Phenotype
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Proto-Oncogene Proteins c-fos / biosynthesis
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Proto-Oncogene Proteins c-fos / genetics
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Proto-Oncogene Proteins c-jun / biosynthesis
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Proto-Oncogene Proteins c-jun / genetics
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Rats
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T-Lymphocytes, Cytotoxic / immunology
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Transfection
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Vaccination
Substances
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Antigens, Neoplasm
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H-2 Antigens
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H-2Kb protein, mouse
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Neoplasm Proteins
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Proto-Oncogene Proteins c-fos
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Proto-Oncogene Proteins c-jun