安田 浩之 (ヤスダ ヒロユキ)

Yasuda, Hiroyuki

写真a

所属(所属キャンパス)

医学部 内科学教室(呼吸器) (信濃町)

職名

准教授

外部リンク

経歴 【 表示 / 非表示

  • 2001年04月
    -
    2005年03月

    慶應義塾大学医学部内科学教室

  • 2005年04月
    -
    2010年12月

    慶應義塾大学医学部内科学(呼吸器)

  • 2011年01月
    -
    2012年03月

    Beth Israel Deaconess Medical Center, Harvard Medical School

  • 2012年04月
    -
    継続中

    慶應義塾大学医学部内科学(呼吸器)

学歴 【 表示 / 非表示

  • 2001年

    慶応義塾大学, 医学部

    卒業

学位 【 表示 / 非表示

  • 医学博士, 慶應義塾大学, 論文

 

研究分野 【 表示 / 非表示

  • ライフサイエンス / 分子生物学 (腫瘍生物学)

  • ライフサイエンス / 細胞生物学 (細胞生物学)

  • ライフサイエンス / 呼吸器内科学 (肺癌)

研究キーワード 【 表示 / 非表示

  • オルガノイド

  • トランスレーショナル研究

  • バイオバンク

  • 細胞生物学

  • 肺癌

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論文 【 表示 / 非表示

  • Initial single-institutional experience with salvage surgery for stage IV non-small-cell lung cancer

    Hishida T., Oka N., Yano K., Omura S., Okubo Y., Masai K., Kaseda K., Ohgino K., Terai H., Yasuda H., Asakura K.

    Interdisciplinary Cardiovascular and Thoracic Surgery 40 ( 3 )  2025年03月

     概要を見る

    The purpose of this study was to assess surgical outcomes of salvage surgery for clinical stage IV non-small-cell lung cancer. A total of 14 patients who underwent lung resection following systemic therapy between 2010 and 2022 were included in this study. Systemic therapy prior to surgery included agents including epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in eight patients and non-TKI agents in six (chemotherapy alone: four, chemotherapy plus immune checkpoint inhibitors: two). During a median follow-up of 5.2 years, the EGFR-TKI group showed a favourable 5-year overall survival of 83%; however, it was due to treatment after relapse, and there were no 4-year relapse-free survivors. The non-EGFR-TKI group showed a 5-year relapse-free survival of 33%, and 2 patients have survived more than 3 years without any relapse and further treatment. When considering the role of surgery in multimodal treatment for initial c-stage IV non-small-cell lung cancer, salvage surgery following non-TKI therapy (chemotherapy with or without immune checkpoint inhibitor) can be regarded as genuine salvage surgery.

  • Celecoxib prevents malignant progression of smoking-induced lung tumors via suppression of the COX-2/PGE<inf>2</inf> signaling pathway in mice

    Sakurai K., Chubachi S., Miyata J., Hamamoto J., Naganuma T., Shimada T., Otake S., Nakayama S., Irie H., Tsutsumi A., Kameyama N., Hegab A.E., Shimoda M., Terai H., Yasuda H., Kanai Y., Arita M., Fukunaga K.

    Frontiers in Immunology 16   1557790 2025年

     概要を見る

    Introduction: Lung cancer is characterized by a poor prognosis and is a significant comorbidity of chronic obstructive pulmonary disease (COPD). Therefore, effective chemopreventive agents are warranted. We evaluated the effects of the cyclooxygenase-2 (COX-2) inhibitor celecoxib on the prevention of lung-carcinoma development using an intermittent smoking-induced lung-carcinoma mouse model. Additionally, we explored COX-2’s role in lipid metabolism. Methods: Male A/J mice were exposed to sham air or mainstream cigarette smoke for 20 weeks. Vehicle or celecoxib was administered via intragastric feeding once daily. Lung tissues were analyzed for tumor nodules and emphysema; the bronchoalveolar lavage fluid was collected for cell counting. COX-2 expression was measured using real-time polymerase chain reaction and western blotting; lipidomic analysis was conducted using liquid chromatography-tandem mass spectrometry. Cell proliferation and colony-forming assays were performed on LA-4 cells to assess the effects of prostaglandins and COX-2 inhibitors. Results: Intermittent smoking exposure increased lung adenomas, adenocarcinomas, and COX-2 expression. Lung adenomas were characterized by abundant COX-2-positive cells. Celecoxib reduced intermittent smoking-induced inflammation, emphysema, and cell counts in the bronchoalveolar lavage fluid and decreased the incidence of lung adenocarcinomas, whereas the total number of observed lung tumors was unchanged. Celecoxib markedly suppressed single-smoke-induced prostaglandin E2 (PGE2) production in the airway. PGE2 increased LA-4 cell viability via the EP4 receptor and promoted colony formation. Discussion: Celecoxib effectively inhibited lung-carcinoma development, inflammation, and emphysema, demonstrating the potential for chemoprevention in smokers and patients with COPD. Further studies on EP4 inhibitors for the prevention of emphysema and lung cancer are warranted.

  • Real-World Efficacy and Safety of Atezolizumab for Advanced Non-Small Cell Lung Cancer in Japan: A Retrospective Multicenter Analysis

    Okada M., Ohgino K., Horiuchi K., Sayama K., Arai D., Watase M., Kobayashi K., Terashima T., Ishioka K., Miyawaki M., Sakamaki F., Masuzawa K., Terai H., Yasuda H., Soejima K., Fukunaga K.

    Journal of Clinical Medicine 13 ( 24 )  2024年12月

    ISSN  2077-0383

     概要を見る

    Background/Objectives: Atezolizumab, an immune checkpoint inhibitor (ICI), was used in a phase III clinical trial, i.e., the OAK trial, of previously treated patients with non-small cell lung cancer. We aimed to evaluate the real-world efficacy and safety of atezolizumab in a non-selected population and identify the clinical characteristics that influence its efficacy. Methods: This was a multicenter, retrospective, single-arm observational study. Seventy-four patients with advanced non-small cell lung cancer, who received atezolizumab monotherapy at Keio University and affiliated hospitals in Japan between April 2018 and March 2019, were enrolled. The follow-up period was until 28 February 2024. The efficacy of treatment and adverse events were reviewed retrospectively. Statistical analyses using Pearson’s χ2 test, Fisher’s exact test, log-rank test, and Student’s t-test were performed. Results: The median age of patients was 70 (range, 45–85) years. The overall survival duration was 7.54 (95% confidence interval [CI], 5.14–11.3) months, and the median time to treatment failure (TTF) was 2.00 (95% CI, 1.75–2.54) months. Patients treated with atezolizumab as their first ICI had a longer TTF than those treated with atezolizumab as their second or subsequent ICI (p = 0.04). Conclusions: Atezolizumab may be more effective when used as the first ICI for previously treated patients and may be safely used in elderly patients with non-small cell lung cancer in real-world settings.

  • Therapeutic Efficacy of IL7/CCL19-Expressing CAR-T Cells in Intractable Solid Tumor Models of Glioblastoma and Pancreatic Cancer

    Ohta K., Sakoda Y., Adachi K., Shinozaki T., Nakajima M., Yasuda H., Nagano H., Tamada K.

    Cancer Research Communications (American Association for Cancer Research (AACR))  4 ( 9 ) 2514 - 2524 2024年09月

     概要を見る

    Cancer immunotherapy using immune checkpoint inhibitors and its combination with other anticancer therapies has emerged as a new standard of care because of the encouraging therapeutic effects in various solid cancers. Nonetheless, glioblastoma and pancreatic cancer remain resistant to immunotherapy and represent intractable cancers with the poorest prognosis. We investigated the therapeutic effects of nextgeneration chimeric antigen receptor (CAR) T cells producing IL7 and chemokine (C-C motif) ligand 19 (CCL19; referred to as 7 × 19 CAR-T) in these intractable cancers. Cytotoxic activities and therapeutic effects of 7 × 19 CAR-T were evaluated in vitro and in vivo, in a model using EGFR variant III (EGFRvIII)-positive glioblastoma and anti-EGFRvIII CAR-T generated from healthy donor peripheral blood mononuclear cells (PBMC), or a model using HER2-positive pancreatic cancer organoids and anti-HER2 CAR-T generated from the same patient's PBMC. Anti-EGFRvIII 7 × 19 CAR-T exhibited cytotoxic activity specific to EGFRvIII-positive tumor, induced complete rejection of glioblastoma with massive T-cell infiltration and tumor cell death in the tumor tissues, and consequently prolonged mouse survival. Anti-HER2 7 × 19 CAR-T demonstrated a potent cytotoxic activity against autologous HER2- positive pancreatic cancer organoids and induced complete rejection of autologous tumor along with prolonged mouse survival. Our results suggest that 7 × 19 CAR-T could become a therapeutic option for glioblastoma and pancreatic cancer. To the best of our knowledge, this is the first study to demonstrate the therapeutic efficacy of next-generation CAR-T in an autologous model using patient-derived tumor organoids and CAR-T generated from the same patient's PBMC, in which unwanted allogeneic immune responses are fully excluded.

  • Development of a Machine Learning-Based Model for Predicting the Incidence of Peripheral Intravenous Catheter-Associated Phlebitis.

    Yasuda H, Rickard CM, Mimoz O, Marsh N, Schults JA, Drugeon B, Kashiura M, Kishihara Y, Shinzato Y, Koike M, Moriya T, Kotani Y, Kondo N, Sekine K, Shime N, Morikane K, Abe T

    Journal of critical care medicine (Universitatea de Medicina si Farmacie din Targu-Mures) 10 ( 3 ) 232 - 244 2024年07月

    ISSN  2393-1809

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総説・解説等 【 表示 / 非表示

  • NSCLCにおける1L nivolumab+ipilimumab後の早期進行の解析 LIGHT-NING(Analysis of early progression after 1L nivolumab + ipilimumab in NSCLC: LIGHT-NING)

    戸井 之裕, 今井 久雄, 山口 哲平, 東 公一, 木島 貴志, 岸 一馬, 渡部 聡, 齋藤 春洋, 高島 雄太, 丹保 裕一, 安田 浩之, 畑地 治, 岡田 守人, 佐藤 悠城, 青江 啓介, 大杉 友之, 飛嶋 雄, 堀之内 秀仁, 大江 裕一郎

    肺癌 ((NPO)日本肺癌学会)  64 ( 5 ) 495 - 495 2024年10月

    ISSN  0386-9628

  • EGFR遺伝子変異陽性肺癌の治療革新と未来展望 EGFR exon 20insの治療薬開発の経緯とこれから

    安田 浩之

    肺癌 ((NPO)日本肺癌学会)  64 ( 5 ) 359 - 359 2024年10月

    ISSN  0386-9628

  • EGFR遺伝子変異陽性非小細胞肺癌患者の血中セルフリーDNAを用いたエピゲノム解析(Epigenome analysis of cell-free DNA in patient with non-small cell lung carcinoma with EGFR mutation)

    中島 真, 安田 浩之, 松谷 哲行, 田 迎, 藤本 真央, 新井 恵吏, 富樫 亮, 関 順彦, 金井 弥栄

    日本病理学会会誌 ((一社)日本病理学会)  113 ( 1 ) 367 - 367 2024年02月

    ISSN  0300-9181

  • CGP検査の結果により遺伝カウンセリング推奨となった胸部悪性腫瘍症例の考察

    福島 貴大, 寺井 秀樹, 中村 康平, 川野 竜太郎, 江本 桂, 石川 麻倫, 緒方 暁彦, 高岡 初誉, 齋藤 彩夏, 扇野 圭子, 安田 浩之, 川田 一郎, 副島 研造, 西原 広史, 福永 興壱

    肺癌 ((NPO)日本肺癌学会)  63 ( 5 ) 461 - 461 2023年10月

    ISSN  0386-9628

  • NKX2-1が規定する肺腺癌のWnt依存性・非依存性(NKX2-1 expression defines Wnt dependency patterns in human lung adenocarcinoma)

    浜本 純子, 江本 桂, 寺井 秀樹, 川田 一郎, 副島 研造, 安田 浩之, 佐藤 俊朗

    日本癌学会総会記事 ((一社)日本癌学会)  82回   1868 - 1868 2023年09月

    ISSN  0546-0476

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競争的研究費の研究課題 【 表示 / 非表示

  • 酸素を用いた癌治療法の開発

    2024年06月
    -
    2027年03月

    安田 浩之, 挑戦的研究(開拓), 補助金,  研究代表者

  • 肺癌オルガノイドライブラリーを用いた肺癌シグナル経路異常の解明

    2021年04月
    -
    2024年03月

    文部科学省・日本学術振興会, 科学研究費助成事業, 安田 浩之, 基盤研究(B), 補助金,  研究代表者

  • 肺癌オルガノイドライブラリー統合解析による癌の不均一性の解明と新規治療標的同定

    2020年04月
    -
    2022年03月

    日本医療研究開発機構(AMED), 次世代がん医療創生研究事業, 安田浩之, 研究代表者

  • 肺癌オルガノイドを用いた治療後期肺癌の悪性度の本態解明

    2019年04月
    -
    2022年03月

    日本医療研究開発機構(AMED), 革新的がん医療実用化研究事業, 安田浩之, 未設定

  • 肺癌オルガノイドライブラリーを用いたprecision medicineの確立と新規治療標的の同定

    2018年11月
    -
    2020年03月

    日本医療研究開発機構(AMED), 次世代がん医療創生研究事業, 安田浩之, 未設定

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受賞 【 表示 / 非表示

  • 武田科学振興財団研究助成金(医学系研究継続助成)

    2019年

    受賞区分: その他

  • 研究奨励賞 日本肺癌学会

    2018年

    受賞区分: 国内学会・会議・シンポジウム等の賞

  • 武田科学振興財団研究助成金(医学系研究)

    2016年

    受賞区分: その他

  • 日本肺癌学会 若手奨励賞

    2015年

  • 第55回 日本呼吸器学会 学会奨励賞

    2015年

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担当授業科目 【 表示 / 非表示

  • 薬理学

    2025年度

  • 腫瘍学

    2025年度

  • 内科学(呼吸器)講義

    2025年度

  • 呼吸器内科学臨床実習

    2025年度

  • 内科学(呼吸器)臨床実習

    2025年度

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所属学協会 【 表示 / 非表示

  • 日本癌治療学会, 

    2021年03月
    -
    継続中
  • 日本癌学会, 

    2020年10月
    -
    継続中
  • International Association for the Study of Lung Cancer, 

    2018年10月
    -
    継続中
  • 日本臨床腫瘍学会, 

    2007年04月
    -
    継続中
  • American Association for Cancer Research, 

    2005年10月
    -
    継続中

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