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KAKEN_17K16063seika.pdf
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Title |
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喫煙誘導マウスモデルにおける肺がん発生機序
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Kana |
キツエン ユウドウ マウス モデル ニ オケル ハイガン ハッセイ キジョ
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Kitsuen yūdō mausu moderu ni okeru haigan hassei kijo
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Mechanism of lung tumorigenesis in smoke exposure mouse model
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中鉢, 正太郎
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チュウバチ, ショウタロウ
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Chūbachi, Shōtarō
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慶應義塾大学・医学部 (信濃町)・助教
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Research team head
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科研費研究者番号 : 90464867
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亀山, 直史
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カメヤマ, ナオフミ
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Kaymeyama, Naofumi
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2019
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科学研究費補助金研究成果報告書
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2018
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喫煙による発癌と気腫発生の双方に関わる機序は未解明であり、肺癌と肺気腫の両病態を同時に評価可能な動物モデルは存在しなかった。我々は、A/Jマウスに対して発癌誘導物質であるNNKを投与後にタバコ煙曝露を間歇的に行い、喫煙誘導性に肺癌と肺気腫が生じるモデルを作製した。間歇曝露群では、3か月間の連続曝露群に比し、肺腺癌の形成が促進し、肺気腫も進行した。さらに、間歇タバ コ煙曝露により形成された肺腺癌では、癌内部と周囲にM2マクロファージが局在していた。本研究結果は気腫を背景肺とした肺癌の予防薬・治療の検討に有用な動物モデルを供するものと考える。
The mechanisms involved in smoke-induced tumorigenesis and emphysema are not fully understood, attributable to a lack of appropriate animal models. Here, we optimized a model of intermittent cigarette smoke induced lung cancer and emphysema in A/J mice treated with NNK, a potent carcinogen. Intermittent CS exposure increased the severity of emphysema and resulted in a higher incidence of adenocarcinomas. Furthermore, intermittent CS exposure elicited a marked increase in M2-polarized macrophages within and near the developed tumors. This model is also suitable for screening putative chemo-preventive agents, and serves as a therapeutic intervention that mimics progressive human lung cancer with emphysema in smokers.
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研究種目 : 若手研究(B)
研究期間 : 2017~2018
課題番号 : 17K16063
研究分野 : 呼吸器内科学
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