<Original Article>p53 and MDM2 co-expression in tobacco and betel chewing-associated oral squamous cell carcinomas
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概要
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Oral cancers of tobacco and betel chewers represents a unique in-vivo model to understand the genotoxic effect of tobacco and betel carcinogens on oncogenes and tumor suppressor genes. Coordinated interactions of p53 and MDM2 play an important role in regulation of critical growth control gene following exposure to DNA damaging agents. The purpose of this study is to determine if the tumor suppressor function of p53 is inactivated by mutation or other alternative mechanisms in carcinogen-induced oral squamous cell carcinoma (SCC), and to investigate the clinicopathological significance of p53 and MDM2 expression. The p53 mutation in oral SCC of tobacco and betel chewers (n=40) was detected by polymerase chain reaction - single strand conformation polymorphism (PCR-SSCP) analysis and immunohistochemistry (IHC) was done to investigate p53 and MDM2 proteins overexpression. The incidence of p53 mutation was relatively low (17.5%), but there was a high prevalence of MDM2 overexpression (72.5%). In the total of 40 cases, IHC phenotype showed p53 positive immunostaining with MDM2 positive immunostaining (p53+/MDM2+) 62.5%, p53 negative immunostaining with MDM2 negative immunostaining (p53-/MDM2-) 15%, p53 positive immunostaining with MDM2 negative immunostaining (p53+/MDM2-) 12.5%, and p53 negative immunostaining with MDM2 positive immunostaining (p53-/MDM2+) 10%. A significant correlation was found between MDM2 and p53 overexpression (p=0.0289). Moreover, p53+/MDM2+ phenotype was significantly associated with poorly differentiated tumors (p=0.0007). These results conclude that other factors than p53 mutation is likely to be the targets of tobacco/betel carcinogens and MDM2 may play an important role in tobacco/betel chewing-related oral SCCs. Overexpression of MDM2 protein may constitute an alternative mechanism for p53 inactivation.
- 東京医科歯科大学の論文
著者
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Takagi Minoru
Department of Anatomy, Nihon University School of Dentistry
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Amagasa T
Tokyo Medical And Dental Univ. Tokyo Jpn
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Amagasa Teruo
Department Of Oral & Maxillofacial Surgery Faculty Of Dentistry Tokyo Medical And Dental Univers
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Amagasa Teruo
Maxillofacial Surgery Maxillofacial Reconstruction And Function Division Of Maxillofacial And Neck R
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Takagi Minoru
Department Of Anatomy Dental Research Center Nihon University School Of Dentistry
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Chiguchi Gaku
Department Of Molecular Cellular Oncology And Microbiology Oral Function Restitution Division Of Ora
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Amagasa Teruo
Department Of Maxillofacial Surgery Graduate School Tokyo Medical And Dental University
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MAUNG Ko
Department of Oral & Maxillofacial Surgery, Institute of Dental Medicine
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Shwe Myint
Department of Molecular Cellular Oncology and Microbiology, Oral Function Restitution, Division of O
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Yamada Shumpei
Department of Maxillofacial Surgery, Maxillofacial Reconstruction and Function, Division of Maxillof
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Nakajima Takuma
Department of Molecular Cellular Oncology and Microbiology, Oral Function Restitution, Division of O
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Tsuchida Nobuo
Department of Molecular Cellular Oncology and Microbiology, Oral Function Restitution, Division of O
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Takagi M
Iwate Fisheries Technol. Center
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Maung Ko
Department Of Oral And Maxillofacial Surgery Institute Of Dental Medicine
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Shwe Myint
Department Of Molecular Cellular Oncology And Microbiology Oral Function Restitution Division Of Ora
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Tsuchida Nobuo
Department Of Molecular Cellular Oncology And Microbiology Tokyo Medical And Dental University
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Tsuchida N
Department Of Molecular Cellular Oncology And Microbiology Oral Function Restitution Division Of Ora
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Yamada Shumpei
Department Of Maxillofacial Surgery Maxillofacial Reconstruction And Function Division Of Maxillofac
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Nakajima Takuma
Department Of Molecular Cellular Oncology And Microbiology Oral Function Restitution Division Of Ora
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Shwe Myint/chiguchi
Department Of Molecular Cellular Oncology And Microbiology Oral Function Restitution Division Of Ora
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