Faculty Profiles - TOMIDA Shuta

MISC - TOMIDA Shuta

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Impact of EGFR-TKI Treatment on the Tumor Immune Microenvironment in EGFR Mutation-Positive Non-Small Cell Lung Cancer. International journal

Kohsuke Isomoto, Koji Haratani, Hidetoshi Hayashi, Shigeki Shimizu, Shuta Tomida, Takashi Niwa, Toshihide Yokoyama, Yasushi Fukuda, Yasutaka Chiba, Ryoji Kato, Junko Tanizaki, Kaoru Tanaka, Masayuki Takeda, Takashi Ogura, Tadashi Ishida, Akihiko Ito, Kazuhiko Nakagawa

Clinical cancer research : an official journal of the American Association for Cancer Research 26 ( 8 ) 2037 - 2046 2020.4

Language：English

PURPOSE: The impact of EGFR tyrosine kinase inhibitors (TKI) on the tumor immune microenvironment (TME) in non-small cell lung cancer (NSCLC) is unclear. EXPERIMENTAL DESIGN: We retrospectively identified 138 patients with EGFR-mutated NSCLC who underwent rebiopsy after progression during EGFR-TKI treatment. PD-L1 and CD73 expression in tumor cells and tumor-infiltrating lymphocyte (TIL) density at baseline and after progression were determined by IHC. Tumor mutation burden (TMB) was determined by next-generation sequencing. RESULTS: The proportion of patients with a PD-L1 expression level of ≥50% (high) increased from 14% before to 28% after EGFR-TKI (P = 0.0010). Whereas CD8+ and FOXP3+ TIL densities were significantly lower after EGFR-TKI treatment than before, CD8+ TIL density was maintained in tumors with a high PD-L1 expression level. Expression of CD73 in tumor cells after EGFR-TKI treatment was higher than that before in patients with a high PD-L1 expression level. TMB tended to be higher after EGFR-TKI treatment than before (3.3→4.1 mutations/Mbp, P = 0.0508). Median progression-free survival for subsequent treatment with antibodies to PD-1 was longer for patients with a high than for those with a low PD-L1 expression after EGFR-TKI (7.1 vs. 1.7 months, P = 0.0033), and two of five patients whose PD-L1 expression level changed from low to high after EGFR-TKI treatment achieved a PFS of >6 months. CONCLUSIONS: EGFR-TKI treatment was associated with changes in the TME of EGFR-mutated NSCLC, and such changes may provide clues for optimization of subsequent PD-1 inhibitor treatment.

DOI： 10.1158/1078-0432.CCR-19-2027

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EGFRチロシンキナーゼ阻害薬のEGFR遺伝子変異陽性進行非小細胞肺癌の腫瘍微小環境への影響

磯本晃佑, 原谷浩司, 林秀敏, 加藤了資, 田中薫, 武田真幸, 中川和彦, 清水重喜, 伊藤彰彦, 冨田秀太, 丹羽崇, 小倉高志, 横山俊秀, 福田泰, 石田直, 千葉康敬, 谷崎潤子

肺癌 60 ( 2 ) 149 - 149 2020.4

がんゲノム医療外来で遺伝性腫瘍が疑われた症例に関する詳細と当院の取り組み

十川麗美, 河内麻里子, 二川摩周, 加藤芙美乃, 蓮岡佳代子, 浦川優作, 坂井美佳, 山本英喜, 山本英喜, 遠西大輔, 冨田秀太, 平沢晃, 平沢晃, 十川麗美

日本人類遺伝学会大会プログラム・抄録集 65th (CD-ROM) 2020

がん遺伝子パネル検査受検を契機にHBOCが判明し本人および血縁者介入につながった一例

十川麗美, 小川千加子, 蓮岡佳代子, 冨田秀太, 井上博文, 松原岳大, 二川摩周, 浦川優作, 河内麻里子, 河内麻里子, 山本英喜, 増山寿, 平沢晃, 平沢晃

日本遺伝性腫瘍学会学術集会プログラム・抄録集 26th 2020

がんゲノム医療に順応する細胞診検査体制~Rapid on-site evaluation:ROSEへの対応~

井上博文, 井上博文, 松岡博美, 實平悦子, 松岡昌志, 冨田秀太, 平沢晃, 柳井広之

日本臨床細胞学会雑誌(Web) 59 2020

Practical impacts of multi-gene cancer profiling on cancer precision medicine and hereditary tumor

山本英喜, 山本英喜, 久保寿夫, 冨田秀太, 遠西大輔, 豊岡伸一, 豊岡伸一, 平沢晃

日本癌学会学術総会抄録集(Web) 79th 2020

ゲノム医療におけるエキスパートパネル【がんゲノム医療中核拠点病院でのエキスパートパネル】岡山大学のエキスパートパネル

柳井広之, 都地友紘, 谷口恒平, 西田賢司, 井上博文, 井上博文, 松岡博美, 平沢晃, 平沢晃, 河内麻里子, 河内麻里子, 山本英喜, 山本英喜, 冨田秀太, 冨田秀太, 遠西大輔

病理と臨床 38 ( 6 ) 2020

FoundationOne CDxから病的意義不明として検出されるバリアントに対する病的意義の再検討

二川摩周, 浦川優作, 十川麗美, 加藤芙美乃, 坂井美佳, 河内麻里子, 山本英喜, 山本英喜, 冨田秀太, 平沢晃, 平沢晃, 二川摩周

日本人類遺伝学会大会プログラム・抄録集 65th (CD-ROM) 2020

[Training Medical Staff with Basic Skills for Data Science in Genomic Medicine].

Shuta Tomida, Mizuki Morita, Noriyuki Yamashita, Akira Hirasawa, Shinichi Toyooka

Yakugaku zasshi : Journal of the Pharmaceutical Society of Japan 140 ( 5 ) 657 - 661 2020

Language：Japanese

The development of specialized training programs for medical personnel, particularly nurses, clinical laboratory technicians, and pharmacists, is considered critical for the promotion of genomic medicine throughout Japan. Specifically, medical personnel skilled at analyzing and understanding high-throughput genomic data are in high demand. In this symposium, we will introduce the basic knowledge and skills necessary for processing genomic data.

DOI： 10.1248/yakushi.19-00217-2

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腫瘍免疫と微小環境 EGFRチロシンキナーゼ阻害薬のEGFR遺伝子変異陽性進行非小細胞肺癌の腫瘍微小環境への影響

磯本晃佑, 原谷浩司, 林秀敏, 清水重喜, 富田秀太, 丹羽崇, 横山俊秀, 福田泰, 千葉康敬, 加藤了資, 谷崎潤子, 田中薫, 武田真幸, 小倉高志, 石田直, 伊藤彰彦, 中川和彦

肺癌 59 ( 6 ) 567 - 567 2019.11

腫瘍免疫と微小環境 EGFRチロシンキナーゼ阻害薬のEGFR遺伝子変異陽性進行非小細胞肺癌の腫瘍微小環境への影響

肺癌 59 ( 6 ) 567 - 567 2019.11

臨床的疑問より発した研究-Reverse translational research High tumor mutation burdenのALK陽性肺癌におけるアレクチニブ早期耐性について

槇本剛, 大橋圭明, 冨田秀太, 二宮貴一朗, 久保寿夫, 頼冠名, 市原英基, 堀田勝幸, 田端雅弘, 豊岡伸一, 木浦勝行

肺癌 59 ( 6 ) 571 - 571 2019.11

バイオバンクでの長期保存生体試料の品質管理標準化のための予備的検討

山本英喜, 松原岳大, 森田瑞樹, 冨田秀太, 豊岡伸一, 平沢晃

臨床病理 67 ( 補冊 ) 283 - 283 2019.10

転移がんに有効なS100A8/A9阻害薬の開発(Novel therapeutic approach based on S100A8/A9-mediated organ tropic cancer metastasis)

木下理恵, 友信奈保子, 山内明, 枝園和彦, 冨田秀太, 村田等, 二見淳一郎, 近藤英作, 豊岡伸一, 阪口政清

日本癌学会総会記事 78回 P - 2252 2019.9

非小細胞肺癌におけるモネンシン併用療法によるEMT関連薬剤耐性の克服(Overcoming EMT-mediated drug resistance with Monensin-based combined therapy in non-small cell lung cancer)

大智宏祐, 諏澤憲, 冨田秀太, 荒木恒太, 宮内俊策, 三浦章博, 武田達明, 難波圭, 枝園和彦, 山本寛斉, 岡崎幹生, 枝園忠彦, 豊岡伸一

日本癌学会総会記事 78回 P - 1139 2019.9

EGFRチロシンキナーゼ阻害薬のEGFR遺伝子変異陽性進行非小細胞肺癌のPD-L1発現率への影響

磯本晃佑, 原谷浩司, 林秀敏, 清水重喜, 冨田秀太, 丹羽崇, 横山俊秀, 福田泰, 千葉康敬, 加藤了資, 谷崎潤子, 田中薫, 武田真幸, 小倉高志, 石田直, 伊藤彰彦, 中川和彦

肺癌 59 ( 4 ) 419 - 419 2019.8

EGFRチロシンキナーゼ阻害薬のEGFR遺伝子変異陽性進行非小細胞肺癌のPD-L1発現率への影響

肺癌 59 ( 4 ) 419 - 419 2019.8

Rapid Acquisition of Alectinib Resistance in ALK-Positive Lung Cancer With High Tumor Mutation Burden. Reviewed International journal

Makimoto G, Ohashi K, Tomida S, Nishii K, Matsubara T, Kayatani H, Higo H, Ninomiya K, Sato A, Watanabe H, Kano H, Ninomiya T, Kubo T, Rai K, Ichihara E, Hotta K, Tabata M, Toyooka S, Takata M, Maeda Y, Kiura K

Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer 14 ( 11 ) 2009 - 2018 2019.7

Language：English

INTRODUCTION: The highly selective ALK receptor tyrosine kinase (ALK) inhibitor alectinib is standard therapy for ALK-positive lung cancers; however, some tumors quickly develop resistance. Here, we investigated the mechanism associated with rapid acquisition of resistance using clinical samples. METHODS: Autopsied samples were obtained from lung, liver, and renal tumors from a 51-year-old male patient with advanced ALK-positive lung cancer who had acquired resistance to alectinib in only 3 months. We established an alectinib-resistant cell line (ABC-14) from pleural effusion and an alectinib/crizotinib-resistant cell line (ABC-17) and patient-derived xenograft (PDX) model from liver tumors. Additionally, we performed next-generation sequencing, direct DNA sequencing, and quantitative real-time reverse transcription polymerase chain reaction. RESULTS: ABC-14 cells harbored no ALK mutations and were sensitive to crizotinib while also exhibiting MNNG HOS transforming gene (MET) gene amplification and amphiregulin overexpression. Additionally, combined treatment with crizotinib/erlotinib inhibited cell growth. ABC-17 and PDX tumors harbored ALK G1202R, and PDX tumors metastasized to multiple organs in vivo, whereas the third-generation ALK-inhibitor, lorlatinib, diminished tumor growth in vitro and in vivo. Next-generation sequencing indicated high tumor mutation burden and heterogeneous tumor evolution. The autopsied lung tumors harbored ALK G1202R (c. 3604 G>A) and the right renal metastasis harbored ALK G1202R (c. 3604 G>C); the mutation thus comprised different codon changes. CONCLUSIONS: High tumor mutation burden and heterogeneous tumor evolution might be responsible for rapid acquisition of alectinib resistance. Timely lorlatinib administration or combined therapy with an ALK inhibitor and other receptor tyrosine-kinase inhibitors might constitute a potent strategy.

DOI： 10.1016/j.jtho.2019.07.017

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Rapid acquired resistance to alectinib in ALK-positive lung cancers with high tumor mutation burden

Kadoaki Ohashi, Go Makimoto, Shuta Tomida, Kazuya Nishii, Shinichi Toyooka, Katsuyuki Kiura

CANCER RESEARCH 79 ( 13 ) 2019.7

病理コンパニオン診断と細胞診がんゲノム医療を考慮した病理検体取扱いについて

井上博文, 冨田秀太, 山本英喜, 柳井広之, 平沢晃

日本臨床細胞学会中国四国連合会会報 ( 34 ) 15 - 15 2019.7

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