1991 Fiscal Year Final Research Report Summary
Expression of tumor GST-pi in oral cancer and drug resistance
| Project/Area Number |
02454461
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
外科・放射線系歯学
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| Research Institution | Sapporo Medical College GRANT-IN-AID FOR SCIENTIFIC RESEARCH (B) |
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Principal Investigator |
ODAJIMA Tetsuyo Sapporo Medical College Department of oral surgery Associate professor, 医学部, 講師 (00177239)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOI Toshikazu Sapporo Medical College Department of oral surgery Assistant professor, 医学部, 助手 (30230634)
HIRATA Shoji Sapporo Medical College Department of oral surgery Assistant professor, 医学部, 助手 (50218781)
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| Project Period (FY) |
1990 – 1991
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| Keywords | oral cancer / GST-pi / drug resistance / malignancy / culture / P-glycoprotein / DNA ploidy / PCNA |
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| Research Abstract |
Significant immunohistochemical activities of GST-pi were more likely to be strongly stained positively as precancerous lesions progress from epithelial hyperplasia to papilloma, dysplasia and carcinoma. GST-pi is likely to prove a useful marker for diagnosis of pre-cancerous lesions.
Twenty-one human tongue carcinomas were analyzed immunohistochemically before and after chemotherapy for the presence of GST-pi and P-glycoprotein, the product of the multiple drug resistance (mdr) gene, which has been associated with resistance to various cytotoxic drugs used in chemotherapeutic treatment. There existed no relationship between response to chemotherapy and expression of p-glycoprotein and GST-pi. Further investigations are planned to pxplore the drug resistance and expressions of mdr and GST-pi in seven oral cancer cell lines.
Using immunocytochemical and biochemichal techniques, we have demonstrated the cultured human oral cancer cell lines (HSC-2, HSC-3 and HSC-4) produce GST-pi. GST-pi content, measured by enzymeimmunoassay in the culture medium, was elevated 4 to 5fold in these cancer cell lines when compared to control non-malignant keratinocyte in primary culture from human gingiva, showing a maximum increase in the subconfluent proliferating period. Moreover, immunoreactivity of GST-pi was significantly higher than in cancer cells compared to control keratinocyte with no GST-pi activity
Expression of GST-pi was studied immunohistochemically for possible correlation with DNA ploidy and expressions of proliferating cell nuclear antigen (PCNA) and tumor surpressor gene product P-53 was studied in 21 patients with oral cancer. No relationship was found between DNA ploidy and expressions of GST-pi and P-53. In contrast, a significant correlation existed between GST-pi and PCNA expressions, suggesting an association of GST-pi with tumor cell proliferation.
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