Details of a Researcher - Yasuda, Hiroyuki

Yasuda, Hiroyuki

写真a

Affiliation: School of Medicine, Department of Internal Medicine (Pulmonary Medicine) (Shinanomachi)

Position: Associate Professor

External Links

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Career 【 Display / hide 】

2001.04

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2005.03

慶應義塾大学医学部内科学教室
2005.04

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2010.12

慶應義塾大学医学部内科学（呼吸器）
2011.01

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2012.03

Beth Israel Deaconess Medical Center, Harvard Medical School
2012.04

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Present

慶應義塾大学医学部内科学（呼吸器）

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Academic Background 【 Display / hide 】

2001

慶応義塾大学, 医学部

Graduated

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Academic Degrees 【 Display / hide 】

医学博士, 慶應義塾大学, Dissertation

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Research Areas 【 Display / hide 】

Life Science / Molecular biology (腫瘍生物学)
Life Science / Cell biology (細胞生物学)
Life Science / Respiratory medicine (肺癌)

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Research Keywords 【 Display / hide 】

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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Papers 【 Display / hide 】

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

Tomoyuki Hishida, Naoyuki Oka, Kaito Yano, Seiji Omura, Yu Okubo, Kyohei Masai, Kaoru Kaseda, Keiko Ohgino, Hideki Terai, Hiroyuki Yasuda, Keisuke Asakura

Interdisciplinary cardiovascular and thoracic surgery 40 ( 3 ) 2025.03

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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.
- Access to Document (DOI)
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

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

Masahiko Okada, Keiko Ohgino, Kohei Horiuchi, Koichi Sayama, Daisuke Arai, Mayuko Watase, Keigo Kobayashi, Takeshi Terashima, Kota Ishioka, Masayoshi Miyawaki, Fumio Sakamaki, Keita Masuzawa, Hideki Terai, Hiroyuki Yasuda, Kenzo Soejima, Koichi Fukunaga

Journal of clinical medicine 13 ( 24 ) 2024.12

ISSN 2077-0383

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

Keisuke Ohta, Yukimi Sakoda, Keishi Adachi, Taro Shinozaki, Masao Nakajima, Hiroyuki Yasuda, Hiroaki Nagano, Koji Tamada

Cancer Research Communications (American Association for Cancer Research (AACR)) 4 ( 9 ) 2514 - 2524 2024.09

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Abstract

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 next-generation 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.

Significance:

Despite the clinical development of CAR T-cell therapy, its efficacy in solid cancers has yet to be established. This study explored the therapeutic potential and immunologic mechanisms of IL7/CCL19-producing CAR-T therapy in preclinical solid cancer models of glioblastoma and pancreatic cancer. We found that IL7/CCL19-producing CAR-T cells generated from the patient’s PBMC showed potent therapeutic effects against the solid cancer model established by inoculating organoids from the autologous tumor tissue.
- Access to Document (DOI)
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 2024.07

ISSN 2393-1809
- Access to Document (DOI)

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Papers, etc., Registered in KOARA 【 Display / hide 】

Identification of lung cancer cell-specific dependent genes or signals using lung cancer organoid library

Yasuda, Hiroyuki

福澤諭吉記念慶應義塾学事振興基金事業報告集 (福澤基金運営委員会) 2023
Identification of signal or gene dependency of lung cancer cells using patient-derived lung cancer organoid library

Yasuda, Hiroyuki

福澤諭吉記念慶應義塾学事振興基金事業報告集 (福澤基金運営委員会) 2022
Establishment of lung cancer and normal lung organoid library

Yasuda, Hiroyuki

科学研究費補助金研究成果報告書 2021
Identification of essential genes or pathways of lung cancer cells using a patient-derived lung cancer organoid library

Yasuda, Hiroyuki

福澤諭吉記念慶應義塾学事振興基金事業報告集 (福澤基金運営委員会) 2021
Translational research for lung cancer biology

Yasuda, Hiroyuki

学事振興資金研究成果実績報告書 (慶應義塾大学) 2020

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Reviews, Commentaries, etc. 【 Display / hide 】

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 2024.10

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 2024.10

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 2024.02

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 2023.10

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 2023.09

ISSN 0546-0476

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

酸素を用いた癌治療法の開発

2024.06

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2027.03

挑戦的研究（開拓）, Principal investigator
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

2021.04

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2024.03

MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), Principal investigator
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

2020.04

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2022.03

日本医療研究開発機構（AMED), 次世代がん医療創生研究事業, Principal investigator
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

2019.04

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2022.03

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, No Setting
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

2018.11

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2020.03

日本医療研究開発機構（AMED）, 次世代がん医療創生研究事業, No Setting, No Setting

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Awards 【 Display / hide 】

武田科学振興財団研究助成金（医学系研究継続助成）

2019

Type of Award： Other
研究奨励賞　日本肺癌学会

2018

Type of Award： Award from Japanese society, conference, symposium, etc.
武田科学振興財団研究助成金（医学系研究）

2016

Type of Award： Other
日本肺癌学会　若手奨励賞

2015
第55回　日本呼吸器学会　学会奨励賞

2015