The Journal of the Korean bone and joint tumor society (대한골관절종양학회지)
- Volume 3 Issue 2
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- Pages.69-79
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- 1997
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- 1226-4962(pISSN)
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- 2233-9841(eISSN)
Apoptosis Detected by in Situ DNA end-extension in Osteosarcomas - In relation to p53 and Bcl-2 expression -
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Park, Yong-Koo
(Department of Pathology, College of Medicine, Kyung Hee University) ;
- Yang, Moon-Ho (Department of Pathology, College of Medicine, Kyung Hee University) ;
- Park, Hye-Rim (Department of Pathology, College of Medicine, Hallym University) ;
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Kim, Youn-Wha
(Department of Pathology, College of Medicine, Kyung Hee University) ;
- Lee, Ju-Hie (Department of Pathology, College of Medicine, Kyung Hee University)
- Published : 1997.08.30
Abstract
Objective : The objective of this study was to compare expression of various proto-oncogenes and rates of apoptosis in osteosarcoma patients. Modulation of apoptosis may influence resistance to chemotherapy and therefore affect the outcome of cancer treatment. Osteosarcoma is one of the most fatal malignancies in young adolescents and investigation of the role of apoptotic cell death is warranted in relation to chemotherapy and tumor outcome. Design : The terminal deoxynucleotidyl transferase to exposed 3'-hydroxyl termini of DNA (TUNEL method) staining method has been applied for the in situ detection of DNA double strand breaks. Patients : Thirty-three osteosarcomas in various stages of differentiation from twenty-nine patients were investigated immunohistochemically for p53, Bcl-2 and TUNEL method for apoptosis. Results and conclusion; We have found that higher level of wild type p53 were correlated with enhanced expression of apoptosis. Increased apoptosis rates were found in cases of negative Bcl-2 expression. In the present study, we have concluded that a significant proportion of osteosarcoma, a tumor in which resistance to chemotherapy often occurs, express high levels of p53 and low levels of Bcl-2. Our data provide further evidence for cross-talk between Bcl-2 and p53 and suggests that these genes are important determinants of drug-induced apoptosis.