2002 Fiscal Year Final Research Report Summary
Alterations of cell adhesion-, growth- and transcription-relating genes in oral squamous cell carcinomas
| Project/Area Number |
13672109
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Surgical dentistry
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
ODAJIMA Tetsuyo Sapporo Medical University School of Medicine Assistant professor, 医学部, 講師 (00177239)
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| Co-Investigator(Kenkyū-buntansha) |
SATOH Masaaki Sapporo Medical University School of Medicine Associate professor, 医学部, 助教授 (40187232)
YOSHIDA Koichi Sapporo Medical University School of Medicine Professor, 医学部, 教授 (60117653)
TANAKA Nobuyuki Sapporo Medical University School of Medicine Associate professor, 医学部, 助教授 (50163548)
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| Project Period (FY) |
2001 – 2002
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| Keywords | oral squamous carcinoma / p53 / cyclin D1 / epidermal growth factor receptor / Rb2 / β-catenin / gene mutation / immunohistochemistry |
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| Research Abstract |
Research 1 : Accumulation of p53, cyclin D1 and epidermal growth factor receptor gene proteins was examined in 140 curatively resected oral squamous cell carcinomas (SCCs). Simul taneous co-expression of all molecular markers was evaluated as an independent prognostic predictor for malignant potential of oral SCCs.
Research 2 : Mutation of Rb2/pl30 gene, a member of the retinoblastoma (Rb) tumor suppressor gene family, was examined in 64 human oral SCCs, together with alteration of the protein expression of pRb2/p130. No mutations involving exons 19 to 22 were detected in 38 oral SCCs and 5 established oral SCC cell lines examined. However, cytoplasmic expression of pRb2 had a prognostic value for patients with oral SCC as well as reduced nuclear expression of the protein.
Research 3 : Mutation of β-catenin gene, a regulator of E-cadherin mediated intercellular adhesion and an activator of signaling in Wnt/Wingless pathways that acts as a oncogene, was examined in 81 oral SCCs. No mutation of β-catenin gene exon 3 was found in oral SCCs, suggesting that mutations of the β-catenin appear to be responsible for oral cancer development. β-catenin seems to play a cell to cell adhesive role that suppresses the detachment of cancer cell from primary tumor site.
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