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KAKEN_17K16851seika.pdf
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Title |
Title |
高悪性度漿液性卵巣癌の発癌初期における分子機構の解明
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Kana |
コウアクセイド ショウエキセイ ランソウガン ノ ハツガン ショキ ニ オケル ブンシ キコウ ノ カイメイ
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Kōakuseido shōekisei ransōgan no hatsugan shoki ni okeru bunshi kikō no kaimei
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Initial steps of high-grade serous ovarian carcinoma carcinogenesis
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中村, 康平
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ナカムラ, コウヘイ
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Nakamura, Kōhei
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慶應義塾大学・医学部 (信濃町) ・特任助教
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Research team head
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科研費研究者番号 : 10775802
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2020
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科学研究費補助金研究成果報告書
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2019
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我々は癌化に必要な3つの遺伝子異常 (p53/KRAS/c-Myc or Akt) を同定し、卵管采上皮不死化細胞株を用いたin vitro発癌モデルを構築し、発癌初期病変であるSerous tubal intraepithelial carcinoma (STIC) におけるシグナル異常の同定を行い、卵管采への排卵時の卵胞液による刺激がHGSOC発癌の初期段階に関与していることが示唆された。また、低悪性度漿液性癌の発癌機序についても、卵巣表層上皮への嚢胞内容液の曝露によるNFkB活性化等が発癌初期イベントに寄与している可能性が示された。
We identified two patterns of three genetic alterations (i.e.,p53/KRASV12/c-Myc and p53/KRASV12/PI3K-AKT) that were essential for HGSOC development, and successfully established an in vitro step-wise model of carcinogenesis using immortalized FTSECs. Furthermore, we identified the signal transduction in STICs and demonstrated that the hormone exposure to fimbriae in ovulation contributes to the initial steps of HGSOC carcinogenesis. Regarding LGSOC carcinogenesis, we demonstrated that the exposure of content fluid of serous cystadenoma to OSE causes the NFkB activation and contributes to the initial steps of LGSOC carcinogenesis.
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研究種目 : 若手研究 (B)
研究期間 : 2017~2019
課題番号 : 17K16851
研究分野 : 卵巣癌、ゲノム
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