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HIMAC炭素イオンビームで誘導されるヒトがん細胞株におけるP53依存的バイスタンダー細胞致死効果

https://repo.qst.go.jp/records/70919
https://repo.qst.go.jp/records/70919
372051bf-dd46-4cd5-b7dc-5e916223e8d1
Item type 会議発表用資料 / Presentation(1)
公開日 2012-09-29
タイトル
タイトル HIMAC炭素イオンビームで誘導されるヒトがん細胞株におけるP53依存的バイスタンダー細胞致死効果
言語
言語 jpn
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 鈴木, 雅雄

× 鈴木, 雅雄

WEKO 696868

鈴木, 雅雄

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鈴木 雅雄

× 鈴木 雅雄

WEKO 696869

en 鈴木 雅雄

Search repository
抄録
内容記述タイプ Abstract
内容記述 We investigated P53-dependent bystander cell-killing effect in human tumor cell lines irradiated with the HIMAC carbon ions. Two cell lines with wild-type P53 and three cell lines with mutated-type P53 were used. Also, two cells transfected with either wild-type P53 (H1299/wtp53) or mutated-type P53 (H1299/mp53) were used. Irradiation was carried out using 4 different protocols; (1) All cells on the dish were irradiated; (2) Irradiated and unirradiated cells were pooled in a 1:1 ratio as a single culture; (3) Half of cells were irradiated using beam stopper; and (4) Half of cells were irradiated with a specific inhibitor of gap-junction. The surviving fraction in the cells with wild-type P53 was the same between the condition (1) and (3). Also, the surviving fraction of (4) was the same with (2). On the other hand, in the cells with mutated-type P53 it was the same level among (2), (3) and (4). The results showed that bystander cell-killing effect was observed in the cells harboring wild-type P53, but not in the P53-mutated cells. Moreover, observed bystander effect was suppressed by treating with a specific inhibitor of gap-junction mediated cell-cell communication.
会議概要(会議名, 開催地, 会期, 主催者等)
内容記述タイプ Other
内容記述 第71回日本癌学会学術総会
発表年月日
日付 2012-09-21
日付タイプ Issued
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