| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1998: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Research Abstract |
We chose 10 cases of colon cancer, 10 cases of colon cancer in adenoma and 10 cases each of colon adenomas, with mild atypia or moderate atypia or severe atypia, respectively. Using the paraffin embedded tissue sections of these cases, we analyzed antigen expression of MHC class I, TAP, HSP72, Calnexin and Grp94 molecules, which related with antigen presentation on the cell surface, by immunohistochemical staining method. The expression of MHC class I antigen decreased on cancer cells compared with normal epithelial cells. However, HSP72, Calnexin and Grp94 molecules expression increased on cancer cells. TAP antibody did not react well to paraffin embedded tissue sections. These data suggested that cancer cells at the very beginning proliferating phase might get immunological tolerance by decreasing MHC class I molecules. Next, we performed quantitative analysis of MHC class I mRNA in colon cancer cells by in situ RT-PCR method. There was no difference between colon cancer cells and normal colon epithelial cells. This suggested that MHC class I molecule expression on cell surface might not be controlled on mRNA level but on protein synthesis step or later steps. We also checked other cancer cells. Maxillary cancer cells also decreased MHC class I molecules expression. In liver cancer cells, we found many LOH (loss of heterozygosity) on various chromosomes except chromosome 6p, on which MHC gene and other MHC-related genes located.
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