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- Material Type
- 文書・図像類
- Title
- Author/Editor
- 仙波, 伊知郎
- Author Heading
- Publication, Distribution, etc.
- Alternative Title
- Analysis for genetic alteration of oral precancerous lesions
- Text Language Code
- jpn
- Target Audience
- 一般
- Note (General)
- 2009-2011年度科学研究費助成事業(科学研究費補助金(基盤研究(C)))研究成果報告書 課題番号：21592337 研究代表者：仙波伊知郎 (鹿児島大学大学院医歯学総合研究科教授)広域発癌の動物モデルとしての口腔扁平上皮の多段階発癌のモデルが確立できたといえ、肉眼変化と組織変化との対応が可能であり、時期と部位差も検討できた。広域発癌における前癌病変は、隆起性の限局病変に対して、び漫性の背景病変として認められる。発がん剤の連続投与では経時的に増強し、浸潤癌の発生まで多段階の過程を経る。一方、発がん剤の投与を中断すると、上皮異形成は減弱するが、現局性隆起病変は発生し、浸潤癌も発生した。さらに、前癌病変におけるDNA二重鎖切断修復に関与する因子の高発現を見いだし、前癌病変段階では、浸潤癌とは異なる発癌過程に重要な因子であることが示唆された。In this study, we successfully established field-cancerization animal model of tongue carcinoma. The model provides well compatibility of macroscopic and microscopic findings and analysis for chronological and site specific changes of the precancerous lesion. In this model, the precancerous lesion shows diffuse epithelial dysplasia and the grade of histological atypia was increased during the carcinogen administration period, although interruption of the administration of the carcinogen brought decrease the atypia but further advanced lesions such as focal protrude lesion and invasive carcinoma. There is high level expression of genes related with double strands DNA damage repair in the precancerous lesions, and it suggests that different properties from in the invasive carcinoma.