Faculty Profiles - TOMIDA Shuta

MISC - TOMIDA Shuta

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Single-Cell DNA Sequencing Reveals Cell-Level Genetic Evolutionary Processes and Clonal Structure in B-Cell Lymphomas

Hiroyuki Murakami, Ryota Chijimatsu, Hideki Ujiie, Yusuke Naoi, Kazutaka Sunami, Kazuhiko Yamamoto, Soichiro Fujii, Tomofumi Yano, Keisuke Seike, Hideaki Fujiwara, Noboru Asada, Nobuharu Fujii, Ken-ichi Matsuoka, Tomohiro Urata, Kazuhiro Ikeuchi, Hiroki Kobayashi, Yasuharu Sato, Shuta Tomida, Yoshinobu Maeda, Daisuke Ennishi

BLOOD 144 1368 - 1369 2024.11

脳腫瘍の分子診断と治療1 Glioblastoma,IDH-wildtype with FGFR gene family alterationsにおける遺伝子変異の検討

家護谷泰仁, 大谷理浩, 劒持直也, 駿河和城, 平野秀一郎, 石田譲治, 藤井謙太郎, 冨田秀太, 遠西大輔, 田中將太

Brain Tumor Pathology 41 ( Suppl. ) 093 - 093 2024.5

がんゲノム医療の次のステップがんゲノム医療の課題と個別化医療の展望肺癌マルチオミクス解析の知見から

豊岡伸一, 枝園和彦, 大亀正義, 冨田秀太, 松岡篤志, 諏澤憲, 山本寛斉, 岡崎幹生, 杉本誠一郎, 遠西大輔

日本外科学会定期学術集会抄録集 124回 WS - 3 2024.4

がんゲノム医療における遺伝性腫瘍の理解とチーム医療のための人材育成の取り組み

蓮岡佳代子, 二川摩周, 加藤芙美乃, 山下範之, 遠西大輔, 冨田秀太, 平沢晃

日本がん看護学会学術集会 38回 262 - 262 2024.2

デジタル空間プロファイラーを用いた肺多形癌の病態解明

松岡篤志, 枝園和彦, 冨田秀太, 水野大輔, 大亀正義, 田中真, 橋本好平, 諏澤憲, 三好健太郎, 山本寛斉, 岡崎幹生, 杉本誠一郎, 遠西大輔, 豊岡伸一

日本呼吸器外科学会総会(Web) 41st 2024

相同組み換え関連遺伝子変異が胃癌の発症年齢や治療効果に与える影響は体細胞と生殖細胞で異なる可能性がある

河野吉泰, 大里俊樹, 堀口繁, 堤康一郎, 遠西大輔, 冨田秀太, 豊岡伸一, 山本英喜, 平沢晃, 大塚基之

日本消化器病学会雑誌(Web) 121 2024

肉腫診療におけるがん遺伝子パネルの有用性

中田英二, 藤原智洋, 国定俊之, 遠西大輔, 山本英喜, 二宮貴一朗, 冨田秀太, 二川摩周, 平沢晃, 豊岡伸一, 尾崎敏文

日本整形外科学会雑誌 97 ( 8 ) S1894 - S1894 2023.8

Musculoskeletal Tumor 骨・軟部腫瘍骨・軟部腫瘍におけるがん遺伝子プロファイリング検査骨・軟部腫瘍診療におけるがん遺伝子パネルの役割

中田英二, 藤原智洋, 国定俊之, 尾崎敏文, 豊岡伸一, 遠西大輔, 山本英喜, 二宮貴一朗, 冨田秀太, 平沢晃, 二川摩周, 田端雅弘

癌と化学療法 50 ( 3 ) 314 - 320 2023.3

[Ⅲ. The Role of Comprehensive Genomic Profiling in Sarcoma].

Eiji Nakata, Tomohiro Fujiwara, Toshiyuki Kunisada, Toshifumi Ozaki, Shinichi Toyooka, Daisuke Ennishi, Hideki Yamamoto, Kiichiro Ninomiya, Shuta Tomida, Akira Hirasawa, Mashu Futagawa, Masahiro Tabata

Gan to kagaku ryoho. Cancer & chemotherapy 50 ( 3 ) 314 - 320 2023.3

Multilayered Regional Collaboration in personalized cancer medicine

十川麗美, 十川麗美, 二川摩周, 加藤芙美乃, 山下範之, 山下範之, 浦川優作, 植野さやか, 深野智華, 山本英喜, 山本英喜, 山本英喜, 冨田秀太, 平沢晃, 平沢晃, 平沢晃

Bio Clinica 38 ( 7 ) 2023

岡大バイオバンク:研究支援を加速するためのDXの推進

松原岳大, 江見裕美, 石田紀子, 岩木麻希子, 窪田弥生, 柴倉美砂子, 那須遥, 福田俊, 室崎眞奈, 山本英喜, 冨田秀太, 遠西大輔, 平沢晃, 森田瑞樹, 豊岡伸一, 山本英喜, 冨田秀太, 遠西大輔, 平沢晃, 森田瑞樹, 豊岡伸一, 山本英喜, 冨田秀太, 平沢晃, 森田瑞樹, 豊岡伸一

日本遺伝子診療学会大会プログラム・抄録集 30th 2023

ゲノム情報を有効に活用するための診療体制の構築

中田英二, 藤原智洋, 国定俊之, 遠西大輔, 二宮貴一朗, 冨田秀太, 二川摩周, 山本英喜, 平沢晃, 田端雅弘, 豊岡伸一, 尾崎敏文

日本整形外科学会雑誌 97 ( 6 ) 2023

岡山大学病院における小児がんゲノム診療の実際と今後の課題

石田悠志, 塩飽孝宏, 為房宏輔, 藤原かおり, 鷲尾佳奈, 遠西大輔, 冨田秀太, 平沢晃, 豊岡伸一, 塚原宏一

中国四国小児科学会プログラム・抄録集 75th (Web) 2023

空間トランスクリプトーム解析による間質性肺炎合併肺癌の病態解明

大亀正義, 枝園和彦, 松岡篤志, 冨田秀太, 東原朋諒, 向原史晃, 林直宏, 土生智大, 吉川真生, 諏澤憲, 山本寛斉, 遠西大輔, 豊岡伸一

日本肺癌学会学術集会号 64th (CD-ROM) 2023

がんゲノム医療における多職種連携の実際

蓮岡佳代子, 冨田秀太, 遠西大輔, 平沢晃

日本臨床外科学会雑誌 84 ( Supplement (Web) ) 2023

EGFR阻害が誘導するEgfr肺癌に対する抗腫瘍免疫を逐次的VEGFR-2/PD-1阻害が増強する

西井和也, 大橋圭明, 冨田秀太, 中須賀崇匡, 平生敦子, 大川祥, 西村淳, 安東千裕, 槇本剛, 二宮貴一朗, 加藤有加, 久保寿夫, 市原英基, 堀田勝幸, 田端雅弘, 豊岡伸一, 鵜殿平一郎, 前田嘉信, 木浦勝行

肺癌 62 ( 6 ) 657 - 657 2022.11

がん遺伝子パネルに基づく肉腫診療

中田英二, 藤原智洋, 平沢晃, 二川摩周, 遠西大輔, 山本英喜, 冨田秀太, 久保寿夫, 田端雅弘, 国定俊之, 豊岡伸一, 尾崎敏文

日本癌治療学会学術集会抄録集 60回 O49 - 4 2022.10

がん遺伝子パネルに基づく肉腫診療

中田英二, 藤原智洋, 平沢晃, 二川摩周, 遠西大輔, 山本英喜, 冨田秀太, 久保寿夫, 田端雅弘, 国定俊之, 豊岡伸一, 尾崎敏文

日本癌治療学会学術集会抄録集 60回 O49 - 4 2022.10

進展型小細胞肺癌における免疫チェックポイント阻害薬の効果と腫瘍微小免疫環境の関連

金村宙昌, 林秀敏, 原谷浩司, 中川和彦, 冨田秀太, 谷崎潤子, 鈴木慎一郎, 川中雄介, 津谷あす香, 福田泰, 金田裕靖, 工藤慶太, 高濱隆幸, 今井亮介, 千葉康敬, 大谷知之, 伊藤彰彦, 坂井和子, 西尾和人

肺癌 62 ( 5 ) 442 - 442 2022.10

学生発、がんゲノムゼミ。実臨床の経験を基にした自発的ゼミの立ち上げと報告

宮崎将司, 宇佐美佳耶, 加藤唯真, 川月章弘, 木山満就, 小堀貴之, 増田倫敦, 遠西大輔, 冨田秀太, 千々松良太, 山下範之, 豊岡伸一

医学教育 53 ( Suppl. ) 223 - 223 2022.7

がん遺伝子パネル検査で検出されたPGPVの特性および遺伝子医療部門への介入方法の検討

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

日本遺伝カウンセリング学会誌 43 ( 2 ) 77 - 77 2022.6

口腔癌間質由来のCCL2はCCR2陽性骨髄由来免疫抑制細胞の腫瘍間質への動員に関与する

河合穂高, メイ・ワトウ, 高畠清文, 冨田秀太, 小野喜章, 江口傑徳, 大原利章, 中野敬介, 長塚仁

日本がん免疫学会総会プログラム・抄録集 26回 91 - 91 2022.6

口腔癌間質由来のCCL2はCCR2陽性骨髄由来免疫抑制細胞の腫瘍間質への動員に関与する

河合穂高, メイ・ワトウ, 高畠清文, 冨田秀太, 小野喜章, 江口傑徳, 大原利章, 中野敬介, 長塚仁

日本がん免疫学会総会プログラム・抄録集 26回 91 - 91 2022.6

Genomic medicine and new treatment strategies based on biomarkers for soft tissue sarcoma

中田英二, 藤原智洋, 国定俊之, 尾崎敏文, 平沢晃, 二川摩周, 遠西大輔, 冨田秀太, 久保寿夫, 宮本理史

整形・災害外科 65 ( 3 ) 2022

プレシジョン・メディシンの時代に呼吸器外科医が果たす役割

枝園和彦, 枝園和彦, 諏澤憲, 山本寛斉, 岡崎幹生, 田中真, 三好健太郎, 杉本誠一郎, 遠西大輔, 冨田秀太, 豊岡伸一

日本呼吸器外科学会総会(Web) 39th 2022

包括的ゲノムプロファイリングを用いた神経内分泌癌の治療探索と生殖細胞系列の推定

山本英喜, 河内麻里子, 堀口繁, 榮浩行, 久保寿夫, 二宮貴一朗, 西森久和, 高本篤, 遠西大輔, 冨田秀太, 宮本理史, 田端雅弘, 柳井広之, 豊岡伸一, 平沢晃

日本癌治療学会学術集会抄録集 59回 O73 - 3 2021.10

消化器領域細胞診への細胞検査士の挑戦胆・膵癌におけるがん遺伝子パネル検査の課題細胞診にできること

井上博文, 松岡博美, 實平悦子, 松岡昌志, 冨田秀太, 松本和幸, 堀口繁, 加藤博也, 山本英喜, 柳井広之, 平沢晃

日本臨床細胞学会雑誌 60 ( Suppl.2 ) 470 - 470 2021.10

小細胞癌のICI(Treatment of SCLC) 進展型小細胞肺癌における腫瘍微小免疫環境の網羅的解析

金村宙昌, 林秀敏, 大谷知之, 冨田秀太, 鈴木慎一郎, 原谷浩司, 谷崎潤子, 津谷あす香, 福田泰, 金田裕靖, 工藤慶太, 高濱隆幸, 今井亮介, 千葉康敬, 西尾和人, 伊藤彰彦, 中川和彦

肺癌 61 ( 6 ) 499 - 499 2021.10

【骨・軟部腫瘍のマネジメント(その1)】診断組織・遺伝子診断肉腫におけるがんゲノム医療の意義

中田英二, 藤原智洋, 国定俊之, 尾崎敏文, 遠西大輔, 冨田秀太, 平沢晃, 二川摩周, 武田達明

別冊整形外科 ( 79 ) 75 - 83 2021.4

Language：Japanese Publisher：(株)南江堂

＜文献概要＞はじめにがんにはさまざまな遺伝子異常を認め,同一のがん種でも発現する遺伝子が異なることが少なくない.最近,次世代シークエンサー(next generation sequencer:NGS)を用いて遺伝子異常を同時多重性(マルチプレックス)に検出するがん遺伝子パネルが登場した.がんゲノム医療では,がん遺伝子パネルで同定した遺伝子変異に基づいて薬剤を選択する,精密医療(precision medicine)が行われる.本稿では,肉腫におけるゲノム医療の意義について述べる.

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Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2021&ichushi_jid=J04037&link_issn=&doc_id=20210514600016&doc_link_id=10.15106%2Fj_besei79_75&url=https%3A%2F%2Fdoi.org%2F10.15106%2Fj_besei79_75&type=%88%E3%8F%91.jp_%83I%81%5B%83%8B%83A%83N%83Z%83X&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00024_2.gif

がんゲノム医療と肺がん

豊岡伸一, 蓮岡佳代子, 久保寿夫, 遠西大輔, 冨田秀太

日本肺癌学会学術集会号 62nd (CD-ROM) 2021

胆・膵癌におけるがん遺伝子パネル検査の課題-細胞診にできること-

井上博文, 井上博文, 井上博文, 松岡博美, 實平悦子, 松岡昌志, 冨田秀太, 松本和幸, 堀口繁, 加藤博也, 山本英喜, 山本英喜, 柳井広之, 平沢晃

日本臨床細胞学会雑誌(Web) 60 2021

がんゲノム医療で見つかるPGPVsの特徴

十川麗美, 山本英喜, 山本英喜, 河内麻里子, 二川摩周, 浦川優作, 遠西大輔, 冨田秀太, 平沢晃, 平沢晃, 平沢晃

日本癌学会学術総会抄録集(Web) 80th 2021

肉腫におけるがん遺伝子パネルによる融合遺伝子の検出

中田英二, 国定俊之, 藤原智洋, 遠西大輔, 冨田秀太, 尾崎敏文, 尾崎敏文

中部日本整形外科災害外科学会雑誌 64 ( 秋季学会 ) 107 - 107 2021

最良のホルマリン固定パラフィン切片の条件と病理組織像からの核酸収量予測システム

井上博文, 井上博文, 井上博文, 冨田秀太

日本癌学会学術総会抄録集(Web) 80th 2021

がんゲノム医療におけるPGPVに対する遺伝子医療部門の取り組み

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, 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, 平沢晃

日本遺伝性腫瘍学会学術集会プログラム・抄録集 27th 2021

Practice and report of genetic education using videos

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

日本遺伝カウンセリング学会誌 42 ( 2 ) 2021

がん遺伝子パネル検査でATMのPresumed Germline Pathogenic Variant(PGPV)が検出された3例

加藤芙美乃, 山本英喜, 山本英喜, 十川麗美, 二川摩周, 浦川優作, 植野さやか, 河内麻里子, 遠西大輔, 冨田秀太, 平沢晃, 平沢晃

日本人類遺伝学会大会(CD-ROM) 66th 2021

最新版!ゲノム診断における細胞診【春秋シリーズ】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, 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 59 ( Suppl.2 ) 480 - 480 2020.11

The activation of YES1 leads to the acquired resistance to neratinib in HER2-amplified breast and lung cancers

Hiromasa Yamamoto, Tatsuaki Takeda, Ken Suzawa, Shuta Tomida, Shunsaku Miyauchi, Kota Araki, Kentaro Nakata, Akihiro Miura, Tadahiko Shien, Yoshihisa Kitamura, Toshiaki Sendo, Shinichi Toyooka

CANCER RESEARCH 80 ( 16 ) 2020.8

チームアプローチで実現するゲノム医療と薬剤師の役割ゲノム医療におけるデータサイエンティストの役割と育成

冨田秀太, 森田瑞樹, 山下範之, 平沢晃, 豊岡伸一

薬学雑誌 140 ( 5 ) 657 - 661 2020.5

Language：Japanese Publisher：(公社)日本薬学会

次世代シークエンサーを用いた遺伝子パネル検査とそのデータ解析はゲノム医療の根幹であるにもかかわらず、その担い手であるデータサイエンティストが極端に不足している。基本的なデータ解析の流れを理解し、解析結果の解釈ができる人材育成が喫緊の課題である。遺伝子パネル検査の流れを概説するとともに、遺伝子変異量(TMB)の概念と遺伝子パネル検査におけるTMBの算出方法について解説した。

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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

EGFR-TKI耐性NSCLCに対するHSP90阻害剤ganetespibの有用性の検討

栗原英祐, 枝園和彦, 鳥越英次郎, 武田達明, 荒木恒太, 宮内俊策, 三浦章博, 高橋優太, 諏澤憲, 山本寛斉, 宗淳一, 冨田秀太, 豊岡伸一

日本呼吸器外科学会雑誌 33 ( 3 ) O17 - 4 2019.4

チームアプローチで実現するゲノム医療と薬剤師の役割ゲノム医療におけるデータサイエンティストの役割と育成

冨田秀太, 森田瑞樹, 山下範之, 平沢晃, 豊岡伸一

日本薬学会年会要旨集 139年会 ( 1 ) 264 - 264 2019.3

肺がんゲノム医療の経験と今後の展望

諏澤憲, 久保寿夫, 冨田秀太, 高橋優太, 枝園和彦, 山本寛斉, 遠西大輔, 田端雅弘, 木浦勝行, 豊岡伸一

日本臨床腫瘍学会学術集会(CD-ROM) 17th 2019

リキッドバイオプシーでBRCA1の生殖細胞系列病的バリアントが示唆され遺伝カウンセリングを通じて確定診断に至った一例

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, 江見裕美, 浦川優作, 河内麻里子, 河内麻里子, 増山寿, 平沢晃, 平沢晃

日本人類遺伝学会大会プログラム・抄録集 64th 2019

肺癌におけるPrecision Medicineの現状と今後の展開肺癌のゲノム異常と治療の課題

豊岡伸一, 枝園和彦, 山本寛斉, 宗淳一, 冨田秀太

日本癌治療学会学術集会抄録集 56回 PD3 - 2 2018.10

デジタルPCR法による呼気濃縮液を用いたEGFR遺伝子診断法の検討

西井和也, 大橋圭明, 田村朋季, 妹尾賢, 狩野裕久, 渡邉洋美, 小田尚廣, 槇本剛, 肥後寿夫, 二宮貴一朗, 加藤有加, 南大輔, 二宮崇, 久保寿夫, 堀田勝幸, 田端雅弘, 冨田秀太, 豊岡伸一, 前田嘉信, 木浦勝行

肺癌 58 ( 6 ) 597 - 597 2018.10

乳がんにおけるネラチニブ耐性化の機序解析(Analyses of the mechanisms of the resistance to neratinib in breast cancer)

武田達明, 山本寛斉, 冨田秀太, 高橋優太, 栗原英祐, 大越祐介, 枝園和彦, 宗淳一, 北村佳久, 千堂年昭, 豊岡伸一

日本癌学会総会記事 77回 839 - 839 2018.9

EGFR変異陽性肺癌におけるLRIG1の抗腫瘍効果(Tumor-suppressive effect of LRIG1 in non-small cell lung cancer harboring mutant EGFR)

鳥越英次郎, 山本寛斉, 阪口政清, 難波圭, 佐藤博紀, 枝園和彦, 諏澤憲, 宗淳一, 冨田秀太, 佃和憲, 三好新一郎, 豊岡伸一

日本癌学会総会記事 77回 940 - 940 2018.9

HER増幅胃癌におけるアファチニブ耐性機序(Acquired resistant mechanism to afatinib in HER2 amplified gastric cancer cells)

吉岡貴裕, 枝園和彦, 難波圭, 冨田秀太, 山本寛斉, 宗淳一, 藤原俊義, 豊岡伸一

日本癌学会総会記事 77回 1449 - 1449 2018.9

腫瘍浸潤リンパ球(TIL)を含んだ腫瘍解離細胞(DTC)の保存

渡邊元嗣, 高橋優太, 冨田秀太, 宗淳一, 松原岳大, 難波圭, 佐藤博紀, 森田瑞樹, 枝園和彦, 山本寛斉, 鵜殿平一郎, 豊岡伸一

日本がん免疫学会総会プログラム・抄録集 22回 161 - 161 2018.7

Therapeutic strategy for lung cancer with HER2 alteration

Shinichi Toyooka, Ken Suzawa, Takashi Ninomiya, Hiromasa Yamamoto, Kazuhiko Shien, Junichi Soh, Shuta Tomida, Katsuyuki Kiura

CANCER SCIENCE 109 817 - 817 2018.1

Gene expression and mutation profiling for cancer of unknown primary

Hidetoshi Hayashi, Shuta Tomida, Yoshihiko Fujita, Yosuke Togashi, Kazuko Sakai, Kazuto Nishio, Kazuhiko Nakagawa

ANNALS OF ONCOLOGY 28 2017.10

肺癌においてペメトレキセドが次のEGFRチロシンキナーゼ阻害剤治療に及ぼす影響

小林祥久, 冨田秀太, 瀬角裕一, 富沢健二, 光冨徹哉

日本癌学会総会記事 76回 J - 3057 2017.9

分子バーコード技術を用いた低頻度多重変異の同定

難波圭, 冨田秀太, 枝園和彦, 山本寛斉, 宗淳一, 佃和憲, 豊岡伸一

日本癌学会総会記事 76回 P - 3052 2017.9

肺がん新治療の展望 HER2異常肺癌に対する治療戦略

豊岡伸一, 諏澤憲, 二宮崇, 山本寛斉, 枝園和彦, 宗淳一, 冨田秀太, 木浦勝行

日本癌学会総会記事 76回 SST6 - 3 2017.9

抗HER2療法耐性におけるYes1の重要性

武田達明, 山本寛斉, 諏澤憲, 冨田秀太, 難波圭, 渡邉元嗣, 枝園和彦, 宗淳一, 佃和憲, 豊岡伸一

日本癌学会総会記事 76回 P - 3366 2017.9

HER2遺伝子異常肺癌に対するマルチキナーゼ阻害剤Afatinb耐性獲得機序の解明

鳥越英次郎, 枝園和彦, 吉岡貴裕, 難波圭, 佐藤博紀, 山本寛斉, 宗淳一, 浅野博昭, 冨田秀太, 佃和憲, 豊岡伸一

肺癌 57 ( 5 ) 441 - 441 2017.9

A comprehensive analysis of autopsied specimens and patient-derived cell lines in ALK-positive lung cancers with rapid acquired resistance to alectinib

Go Makimoto, Kadoaki Ohashi, Kazuya Nishii, Shuta Tomida, Hiroe Kayatani, Tomoki Tamura, Hisao Higo, Kiichiro Ninomiya, Takashi Ninomiya, Toshio Kubo, Eiki Ichihara, Akiko Sato, Katsuyuki Hotta, Masahiro Tabata, Katsuyuki Kiura

CANCER RESEARCH 77 2017.7

Acquired resistance to the third-generation EGFR inhibitor ASP8273 is associated with MET or NRAS gene amplifications in preclinical models

Kiichiro Ninomiya, Kadoaki Ohashi, Shuta Tomida, Hiroe Kayatani, Tomoki Tamura, Hisao Higo, Go Makimoto, Takashi Ninomiya, Toshio Kubo, Eiki Ichihara, Akiko Sato, Katsuyuki Hotta, Masahiro Tabata, Katsuyuki Kiura

CANCER RESEARCH 77 2017.7

Lung Cancer Panelを用いた多発小型肺癌のマルチプレックス遺伝子変異解析

枝園和彦, 冨田秀太, 佐藤博紀, 高橋優太, 諏澤憲, 山本寛斉, 宗淳一, 三好新一郎, 豊岡伸一

日本呼吸器外科学会雑誌 31 ( 3 ) RO16 - 4 2017.4

十二指腸上皮性腫瘍の遺伝子発現解析の臨床応用の展望

坂口賀基, 山道信毅, 冨田秀太, 高橋悠, 竹内千尋, 小池和彦

Gastroenterological Endoscopy 59 ( Suppl.1 ) 962 - 962 2017.4

Detection of Multiple Low-Frequency Mutations by Molecular-Barcode Sequencing

Kei Namba, Shuta Tomida, Hidejiro Torigoe, Hiroki Sato, Kazuhiko Shien, Hiromasa Yamamoto, Junichi Soh, Kazunori Tsukuda, Shinichiro Miyoshi, Shinichi Toyooka

JOURNAL OF THORACIC ONCOLOGY 12 ( 1 ) S531 - S531 2017.1

Targeting miR-200c/LIN28B Axis in Acquired EGFR-TKI Resistance Non-Small Cell Lung Cancer Cells Harboring EMT Features

Kazuhiko Shien, Hiroki Sato, Ken Suzawa, Shuta Tomida, Shinsuke Hashida, Hiromasa Yamamoto, Junichi Soh, Hidejiro Torigoe, Kei Namba, Mototsugu Watanabe, Hiroaki Asano, Kazunori Tsukuda, Shinichiro Miyoshi, Shinichi Toyooka

JOURNAL OF THORACIC ONCOLOGY 12 ( 1 ) S1267 - S1267 2017.1

Precision Medicine

Tomida Shuta, Toyooka Shinichi

Okayama Igakkai Zasshi (Journal of Okayama Medical Association) 129 ( 1 ) 59 - 60 2017

EGFR変異を有する肺癌細胞株における第三世代EGFR-TKI耐性機序の検討

二宮貴一朗, 大橋圭明, 冨田秀太, 二宮崇, 久保寿夫, 市原英基, 堀田勝幸, 田端雅弘, 谷本光音, 木浦勝行

日本臨床腫瘍学会学術集会(CD-ROM) 15th 2017

非小細胞肺がんにおける受容体型チロシンキナーゼ遺伝子変異の機能解析

寺嶋雅人, 冨樫庸介, 佐藤克明, 水内寛, 坂井和子, 須田健一, 中村雄, 坂野恵里, 林秀敏, デベラス・マルコ, 藤田至彦, 冨田秀太, 光冨徹哉, 西尾和人

近畿大学医学雑誌 41 ( 3-4 ) 20A - 20A 2016.12

非小細胞肺がんにおける受容体型チロシンキナーゼ遺伝子変異の機能解析

寺嶋雅人, 冨樫庸介, 佐藤克明, 水内寛, 坂井和子, 須田健一, 中村雄, 坂野恵里, 林秀敏, デベラス・マルコ, 藤田至彦, 冨田秀太, 光冨徹哉, 西尾和人

近畿大学医学雑誌 41 ( 3-4 ) 20A - 20A 2016.12

NSCLCにおける分子バーコードシークエンス分析による複数の低頻度変異の検出(Detection of multiple low-frequency mutations by molecular-barcode sequencing in NSCLC)

難波圭, 冨田秀太, 枝園和彦, 鳥越英次郎, 佐藤博紀, 山本寛斉, 宗淳一, 佃和憲, 三好新一郎, 豊岡伸一

肺癌 56 ( 6 ) 639 - 639 2016.11

Detection of EGFR mutations in circulating cell-free DNA of non-small cell lung cancer patients by next-generation sequencing

Ken Suzawa, Shuta Tomida, Takahiro Matsubara, Kadoaki Ohashi, Yuho Maki, Hiromasa Yamamoto, Mizuki Morita, Junichi Soh, Hiroaki Asano, Kazunori Tsukuda, Katuyuki Kiura, Shinichiro Miyoshi, Shinichi Toyooka

CANCER RESEARCH 76 2016.7

非ビタミンK阻害経口抗凝固薬の有効性と安全性に関する臨床疫学研究

大島礼子, 小山敏広, 座間味義人, 小川愛子, 森田瑞樹, 冨田秀太, 樋之津史郎, 狩野光伸

日本計量生物学会年会講演予稿集 2016 41‐46 2016

Afatinib activity against head-and-neck or esophageal squamous cell carcinoma: Significance of activating oncogenic HER4 mutations in head-and-neck squamous cell carcinoma

Y. Togashi, Y. Nakamura, S. Tomida, H. Hayashi, M. A. de Velasco, K. Sakai, Y. Fujita, S. Hamada, K. Nishio

ANNALS OF ONCOLOGY 26 97 - 97 2015.12

Integrative algorithm to determine the metastatic carcinoma tissue of origin using next generation sequencing (NGS)

Hidetoshi Hayashi, Shuta Tomida, Yosuke Togashi, Kazuko Sakai, Yoshihiko Fujita, Junji Tsurutani, Issei Kurahashi, Takayasu Kurata, Kazuhiko Nakagawa, Kazuto Nishio

ANNALS OF ONCOLOGY 26 86 - 86 2015.11

EGFR and HER2 signals play a salvage role in MEK1-mutated gastric cancer after MEK inhibition

Takuro Mizukami, Yosuke Togashi, Shunsuke Sogabe, Marco A. de Velasco, Kazuko Sakai, Yoshihiro Fujita, Shuta Tomida, Takako Eguchi Nakajima, Narikazu Boku, Kazuto Nishio

ANNALS OF ONCOLOGY 26 129 - 129 2015.11

非小細胞肺がんにおけるDDR2変異の機能解析

寺嶋雅人, 冨樫庸介, 坂井和子, 佐藤克明, 須田健一, 水上拓郎, 坂野恵里, 中村雄, De Velasco Marco, 藤田至彦, 冨田秀太, 光冨徹哉, 西尾和人

日本癌学会総会記事 74回 P - 2223 2015.10

非小細胞肺がんにおけるDDR2変異の機能解析

寺嶋雅人, 冨樫庸介, 坂井和子, 佐藤克明, 須田健一, 水上拓郎, 坂野恵里, 中村雄, De Velasco Marco, 藤田至彦, 冨田秀太, 光冨徹哉, 西尾和人

日本癌学会総会記事 74回 P - 2223 2015.10

トランスレーショナルリサーチ基礎から臨床応用へ EGFRチロシンキナーゼ阻害剤に対する獲得耐性の機序

豊岡伸一, 諏澤憲, 冨田秀太, 牧佑歩, 山本寛斉, 宗淳一, 三好新一郎

肺癌 55 ( 5 ) 359 - 359 2015.10

The diversity and host interactions of Propionibacterium acnes bacteriophages on human skin (vol 9, pg 2092, 2015)

Jared Liu, Riceley Yan, Qiao Zhong, Sam Ngo, Nathanael J. Bangayan, Lin Nguyen, Timothy Lui, Minghsun Liu, Marie C. Erfe, Noah Craft, Shuta Tomida, Huiying Li

ISME JOURNAL 9 ( 9 ) 2116 - 2116 2015.9

Fibroblast growth factor 9 gene amplification can induce resistance to anti-EGFR therapy in colorectal cancer

T. Mizukami, Y. Togashi, E. Banno, M. Terashima, M. A. De Velasco, K. Sakai, H. Hayashi, Y. Fujita, S. Tomida, T. Eguchi Nakajima, N. Boku, A. Ito, K. Nakagawa, K. Nishio

EUROPEAN JOURNAL OF CANCER 51 S46 - S46 2015.9

Clinicopathological and genetic differences between low-grade and high-grade colorectal mucinous adenocarcinoma

Y. Togashi, Y. Yoshioka, T. Chikugo, M. Terashima, T. Mizukami, H. Hayashi, K. Sakai, M. De Velasco, S. Tomida, Y. Fujita, K. Okuno, K. Nishio

EUROPEAN JOURNAL OF CANCER 51 S390 - S390 2015.9

Activin signal promotes cancer progression and is involved in cachexia in a subset of pancreatic cancer

Yosuke Togashi, Akihiro Kogita, Hiroki Sakamoto, Hidetoshi Hayashi, Masato Terashima, Marco A. de Velasco, Kazuko Sakai, Yoshihiko Fujita, Shuta Tomida, Masayuki Kitano, Masatoshi Kudo, Kazuto Nishio

CANCER RESEARCH 75 2015.8

FGF9 gene amplification can induce resistance to anti-EGFR therapy in colorectal cancer

Takuro Mizukami, Yosuke Togashi, Eri Banno, Masato Terashima, Marco A. de Velasco, Kazuko Sakai, Yoshihiko Fujita, Shuta Tomida, Takako Eguchi Nakajima, Narikazu Boku, Kazuto Nishio

CANCER RESEARCH 75 2015.8

バイオマーカー探索におけるbioinformaticsの役割

冨田秀太, 坂井和子, 西尾和人

がん分子標的治療 13 ( 1 ) 113 - 118 2015.4

Language：Japanese Publisher：(株)メディカルレビュー社

本邦でも急速に普及している次世代シーケンサー(NGS)は、一塩基置換や挿入・欠失といった塩基配列解析のみならず、エクソンレベルの発現解析やバリアントの有無、それらを統合したコピー数解析やリアレンジメントの解析、さらにはエピゲノム解析までを同一プラットフォームで解析することを可能としている。その網羅性・汎用性の高さから、バイオマーカー探索としての利用が進む一方で、蓄積されるデータをいかに解析するかというデータ解析系(ドライ)の問題が最重要課題として認識されつつある。本稿では、今後増加が予想されるNGSを用いたバイオマーカー探索におけるbioinformaticsの役割、特にネットワーク解析について概説する。(著者抄録)

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【ゲノム解析に基づく新しい分子標的治療】次世代型コンパニオン診断薬の創出を目指したゲノム解析

冨田秀太, 坂井和子, 西尾和人

がん分子標的治療 12 ( 4 ) 382 - 387 2015.1

Language：Japanese Publisher：(株)メディカルレビュー社

今日、分子標的薬の開発において、コンパニオン診断薬の同時開発はきわめて重要な課題である。本稿では、(1)FFPEサンプルを対象とした網羅的かつ探索的ながん関連遺伝子変異解析、(2)極微量のサンプルを対象とした既知の遺伝子変異パネルの解析、(3)血液サンプルを対象とした遺伝子変異の(時系列)モニタリング解析に関して概説する。いずれも実用化(臨床応用)された、もしくは実用化間近の解析技術である。これらの解析技術を用いた最新の報告や論文と併せて、次世代型コンパニオン診断薬の創出を目指した最近の動向を概説する。(著者抄録)

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Homozygous deletion of the activin A receptor, type IB gene is associated with an aggressive cancer phenotype in pancreatic cancer

Yosuke Togashi, Hiroki Sakamoto, Hidetoshi Hayashi, Masato Terashima, Marco A. de Velasco, Yoshihiko Fujita, Yasuo Kodera, Kazuko Sakai, Shuta Tomida, Masayuki Kitano, Masatoshi Kudo, Kazuto Nishio

CANCER RESEARCH 74 ( 19 ) 2014.10

MEK INHIBITORS ARE EFFECTIVE AGAINST GASTRIC CANCER CELL LINES WITH ONCOGENIC MEK1 GENE MUTATIONS

Yosuke Togashi, Shunsuke Sogabe, Hiroaki Kato, Masato Terashima, Hidetoshi Hayashi, Kazuko Sakai, Yoshihiko Fujita, Shuta Tomida, Takushi Yasuda, Kazuto Nishio

ANNALS OF ONCOLOGY 25 2014.10

新規ALK阻害剤であるアレクチニブはMET阻害剤との併用で効果が高まる

冨樫庸介, 林秀敏, 寺嶋雅人, 坂井和子, 藤田至彦, 冨田秀太, 中川和彦, 西尾和人

肺癌 54 ( 5 ) 403 - 403 2014.10

喫煙によるニコチン曝露はEGFR遺伝子変異陽性肺がんにおいてEGFR-TKIの耐性因子である

林秀敏, 冨樫庸介, 岡本邦男, 田中妙, 文田壮一, 新谷亮多, 清川寛文, 坂本洋一, 寺嶋雅人, de Velasco Marco A, 坂井和子, 藤田至彦, 冨田秀太, 加藤元一, 中川和彦, 西尾和人

肺癌 54 ( 5 ) 626 - 626 2014.10

CHRONIC NICOTINE EXPOSURE MEDIATES RESISTANCE TO EGFR-TKI IN EGFR-MUTATED LUNG CANCER VIA EGFR SIGNAL

Hidetoshi Hayashi, Yosuke Togashi, Kunio Okamoto, Soichi Fumita, Masato Terashima, Kazuko Sakai, Yoshihiko Fujita, Shuta Tomida, Kazuhiko Nakagawa, Kazuto Nishio

ANNALS OF ONCOLOGY 25 2014.10

原発性肺癌における受容体型チロシンキナーゼAxlの発現と病理組織学的因子の検討

佐藤克明, 清水重喜, 須田健一, 水内寛, 小林祥久, 下治正樹, 富沢健二, 武本智樹, 岩崎拓也, 阪口全宏, 坂井和子, 冨田秀太, 西尾和人, 光冨徹哉

肺癌 54 ( 5 ) 389 - 389 2014.10

低酸素はALK融合遺伝子を有するH3122肺癌細胞株のALK阻害剤に対する耐性化を誘導する

冨樫庸介, 林秀敏, 寺嶋雅人, 坂井和子, 藤田至彦, 冨田秀太, 中川和彦, 西尾和人

肺癌 54 ( 5 ) 470 - 470 2014.10

KIAA1199はグリコーゲンホスホリラーゼキナーゼβサブユニットと結合してグリコーゲンの分解さらには細胞生存を亢進する(KIAA1199 interacts with PHKB and promotes glycogen breakdown and cancer cell survival)

寺嶋雅人, 藤田至彦, 冨樫庸介, 坂井和子, 冨田秀太, 西尾和人

日本癌学会総会記事 73回 P - 2211 2014.9

上皮間葉転換したEGFR-TKI耐性HCC4006におけるABCB1過剰発現は微小管作用薬の交差耐性を誘導する(ABCB1 overexpression in EGFR-TKI resistant HCC4006 cells with EMT feature causes cross-resistant to anti-tubulin agents)

水内寛, 須田健一, 冨田秀太, 佐藤克明, 小林祥久, 下治正樹, 富沢健二, 武本智樹, 岩崎拓也, 阪口全宏, 西尾和人, 光冨徹哉

日本癌学会総会記事 73回 E - 1107 2014.9

MEK遺伝子変異を有する胃がんに対するMEK阻害剤の有効性(MEK inhibitor for gastric cancer with MEK1 gene mutations)

冨樫庸介, 加藤寛章, 林秀敏, 寺嶋雅人, デベラスコ・マルコ, 坂井和子, 藤田至彦, 冨田秀太, 安田卓司, 西尾和人

日本癌学会総会記事 73回 P - 2349 2014.9

EGFR-TKI獲得耐性の分子生物学的・病理学的進展 T790M変異と小細胞肺癌形質転換(Molecular and pathological evolution in acquisition of resistance to EGFR-TKI-T790M mutation and SCLC transformation)

須田健一, 村上功, 佐藤克明, 冨田秀太, 水内寛, 坂井和子, 清水重喜, 富沢健二, 武本智樹, 阪口全宏, 西尾和人, 谷田部恭, 光冨徹哉

日本癌学会総会記事 73回 E - 1108 2014.9

Serum biomarker analysis of WJOG4107: A randomized phase II trial of adjuvant chemotherapy with S-1 versus CDDP+S-1 for resected stage II-IIIA non-small cell lung cancer (NSCLC).

Tetsuya Mitsudomi, Yasuo Iwamoto, Shuta Tomida, Kazuko Sakai, Takeharu Yamanaka, Hirohito Tada, Hiroshige Yoshioka, Kazuya Uchino, Ichiro Yoshino, Shunichi Sugawara, Shigeki Mitsuoka, Toshiaki Takahashi, Mitsunori Ohta, Takashi Seto, Shinji Atagi, Morihito Okada, Hideo Saka, Kazuhiko Nakagawa, Yoichi Nakanishi, Kazuto Nishio

JOURNAL OF CLINICAL ONCOLOGY 32 ( 15 ) 2014.5

【常在細菌叢が操るヒトの健康と疾患】 (第2章)健康を制御する常在細菌叢の新たなバイオロジー皮膚細菌叢のバイオロジー

冨田秀太, 西尾和人, Li Huiying

実験医学 32 ( 5 ) 739 - 743 2014.3

Language：Japanese Publisher：(株)羊土社

体の表面を覆っている皮膚は最大の臓器であり、頭皮から足の裏まできわめて多様で特徴的な組織を有している。その結果、皮膚の細菌叢(スキンマイクロバイオーム)もそれぞれのニッチに適合した、きわめてユニークなコミュニティーを形成していることが、近年のシーケンス技術の飛躍とともに明らかとなってきた。さらに、皮膚の細菌叢とホスト(宿主)間の相互作用メカニズムが徐々に解明され始めており、今後の展開と新しいメカニズムに基づく治療の可能性が注目を集めている。(著者抄録)

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MEK1遺伝子変異を有する胃がん細胞株に対するMEK阻害剤の有効性と臨床サンプルの検討

冨樫庸介, 曽我部俊介, 加藤寛章, 寺嶋雅人, 林秀敏, 林秀敏, 坂井和子, 藤田至彦, 冨田秀太, 安田卓志, 西尾和人

日本臨床腫瘍学会学術集会(CD-ROM) 12th 2014

肺癌生物像に基づいた、新しい肺癌治療の戦略 EGFR遺伝子変異を有する肺癌においてβカテニンを阻害することでEGFR-TKIの効果が増強する

冨樫庸介, 林秀敏, 寺嶋雅人, 藤田至彦, 坂井和子, 冨田秀太, 中川和彦, 西尾和人

肺癌 53 ( 5 ) 397 - 397 2013.10

NGSによる極微量検体を用いたmultiplex mutation analysisの最適化(Optimization of multiplex mutation analysis based on minimum amount of lung cancer specimen)

冨田秀太, 坂井和子, 藤田至彦, 寺嶋雅人, 富樫庸介, デベラスコ・マルコ, 光冨徹哉, 中川和彦, 西尾和人

日本癌学会総会記事 72回 458 - 458 2013.10

【ゲノム医学・生命科学研究総集編ポストゲノムの10年は何をもたらしたか】 (第4章)腸内細菌叢を中心とするマイクロバイオーム皮膚のマイクロバイオーム研究最前線

富田秀太, 西尾和人, Li Huiying

実験医学 31 ( 15 ) 2527 - 2532 2013.9

Language：Japanese Publisher：(株)羊土社

体の表面を覆っている皮膚は適切な細菌との相互作用を利用することにより、そのバリアとしての機能を維持している器官である。サンプルから直接ゲノムDNAを抽出するメタゲノム解析手法と近年の塩基配列解析技術の著しい向上があいまって、皮膚の細菌叢(スキンマイクロバイオーム)の解明とその機能解析が可能となりつつある。本稿では米国国立衛生研究所(National Institutes of Health:NIH)によるHuman Microbiome Project(HMP)に参加したわれわれの体験を踏まえて、最新のスキンマイクロバイオームの研究を中心に、その現状と今後の展開を紹介する。(著者抄録)

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Recent advances in skin microbiome studies

Experimental Medicine 31 ( 15 ) 215 - 220 2013.9

個別化multiplexの体外診断薬承認に向けて

坂井和子, 冨田秀太, 光冨徹哉, 中川和彦, 西尾和人

日本がん分子標的治療学会学術集会プログラム・抄録集 17th 2013

HER2変異肺癌に対するHER2キナーゼ阻害薬耐性機序

富沢健二, 須田健一, 水内寛, 冨田秀太, 森俊輔, 千葉眞人, 小林祥久, 伊藤志門, 宇佐美範恭, 波戸岡俊三, 桑野博行, 光冨徹哉

肺癌 52 ( 5 ) 562 - 562 2012.10

miRNAとmRNAの統合解析による肺腺癌の多様性の検討(Combined analysis of miRNA and mRNA expression towards better understanding of heterogeneities in lung adenocarcinoma)

有馬千夏, 玉田嘉紀, 梶野泰祐, 島田友香子, 井元清哉, 冨田秀太, 宮野悟, 高橋隆

日本癌学会総会記事 71回 254 - 254 2012.8

NKX2-1/TITF1/TTF-1-induced ROR1 is required to sustain EGFR survival signaling in lung adenocarcinoma

Tomoya Yamaguchi, Kiyoshi Yanagisawa, Ryoji Sugiyama, Yasuyuki Hosono, Yukako Shimada, Chinatsu Arima, Seiichi Kato, Shuta Tomida, Motoshi Suzuki, Hirotaka Osada, Takashi Takahashi

CLINICAL CANCER RESEARCH 18 ( 10 ) 2012.5

NKX2-1/TITF1/TTF-1-induced ROR1 is required to sustain EGFR survival signaling in lung adenocarcinoma

Tomoya Yamaguchi, Kiyoshi Yanagisawa, Ryoji Sugiyama, Yasuyuki Hosono, Yukako Shimada, Chinatsu Arima, Seiichi Kato, Shuta Tomida, Motoshi Suzuki, Hirotaka Osada, Takashi Takahashi

CANCER RESEARCH 72 2012.4

マイクロRNA発現プロファイルが示す肺腺癌の多様性(miRNA expression profile-defined heterogeneity in lung adenocarcinoma)

有馬千夏, 冨田秀太, 谷田部恭, 高橋隆

日本癌学会総会記事 70回 141 - 141 2011.9

肺癌におけるPOLD4の関与(Regulation of DNA polymerase subunit POLD4 influences genomic instability in lung cancer)

鈴木元, 冨田秀太, 有馬千夏, 増田雄司, 神谷研二, 長田啓隆, 谷田部恭, 高橋隆

日本癌学会総会記事 70回 102 - 102 2011.9

MYBPH, a novel transcriptional target of TTF-1/NKX2-1, inhibits ROCK1 and actomyosin assembly, and reduces cell motility and tumor metastasis

Yasuyuki Hosono, Tomoya Yamaguchi, Eri Mizutan, Kiyoshi Yanagisawa, Chinatsu Arima, Shuta Tomida, Yukako Shimada, Michiyo Hiraoka, Seiichi Kato, Kohei Yokoi, Motoshi Suzuki, Takashi Takahashi

CANCER RESEARCH 71 2011.4

Roles of ASH1-miR-375 pathway in development of lung cancers with neuroendocrine features

Osada Hirotaka, Eri Nishikawa, Chinatsu Arima, Yasumasa Okazaki, Shuta Tomida, Yoshio Tatematsu, Ayumu Taguchi, Yukako Shimada, Kiyoshi Yanagisawa, Shinya Toyokuni, Yoshitaka Sekido, Takashi Takahashi

CANCER RESEARCH 71 2011.4

肺小細胞癌に見られたPOLD4低発現(Implications of POLD4 regulation and genomic instability in small cell lung cancer)

鈴木元, 冨田秀太, 有馬千夏, 増田雄司, 神谷研二, 長田啓隆, 谷田部恭, 黄勤びょう, 高橋隆

日本癌学会総会記事 69回 525 - 525 2010.8

PCNA Mono-Ubiquitination and Activation of Translesion DNA Polymerases by DNA Polymerase alpha (vol 146, pg 13, 2009)

Motoshi Suzuki, Atsuko Niimi, Siripan Limsirichaikul, Shuta Tomida, Qin Miao Huang, Shunji Izuta, Jiro Usukura, Yasutomo Itoh, Takashi Hishida, Tomohiro Akashi, Yoshiyuki Nakagawa, Akihiko Kikuchi, Youri Pavlov, Takashi Murate, Takashi Takahashi

JOURNAL OF BIOCHEMISTRY 148 ( 2 ) 261 - 261 2010.8

バイオインフォマティクス手法を用いた肺癌のトランスクリプトームおよびプロテオーム解析(Bioinformatic analysis of transcriptome and proteome for lung cancer patients)

冨田秀太, 柳澤聖, 衣斐寛倫, 竹内俊幸, 有馬千夏, 松尾恵太郎, 長田啓隆, 光冨徹哉, 谷田部恭, 高橋隆

日本癌学会総会記事 69回 53 - 53 2010.8

肺腺癌の術後予後の高精度予測を可能とする発現シグネチャーの同定(Relapse-Related Molecular Signature in Lung Adenocarcinomas)

有馬千夏, 冨田秀太, 竹内俊幸, 島田友香子, 松尾恵太郎, 光冨徹哉, 谷田部恭, 高橋隆

日本癌学会総会記事 68回 454 - 455 2009.8

新規遺伝子ADw1は上皮細胞間接着に関与し、肺癌で高頻度に発現低下する(ADw1, a novel gene, is frequently inactivated in lung cancer and involved in cell-cell contact)

長田啓隆, 立松義朗, 冨田秀太, 谷田部恭, 堀尾芳嗣, 樋田豊明, 藤井万紀子, 村上秀樹, 近藤豊, 関戸好孝, 高橋隆

日本癌学会総会記事 67回 298 - 298 2008.9

ASH1 gene may be prototypic "lineagesurvival oncogene" and specific therapeutic target for lung cancers with neuroendocrine features

Hirotaka Sada, Yoshio Tatematsu, Toshiyuki Takeuchi, Shuta Tomida, Hideki Murakami, Yutaka Kondo, Yasushi Yatabe, Yoshitaka Sekido, Takashi Takahashi

JOURNAL OF GENE MEDICINE 10 ( 4 ) 459 - 459 2008.4

In silico screening of differentially expressed microRNAs in lung cancer

Shuta Tomida, Koyo Tsujikawa, Takashi Takahashi

MOLECULAR CANCER THERAPEUTICS 6 ( 12 ) 3486S - 3486S 2007.12

神経内分泌分化誘導因子ASH1によるWntシグナル抑制因子DKK1の発現抑制

長田啓隆, 立松義朗, 竹内俊幸, 冨田秀太, 谷田部恭, 関戸好孝, 高橋隆

日本生化学会大会・日本分子生物学会年会合同大会講演要旨集 80回・30回 3T18 - 4 2007.11

ヒト肺腺癌におけるTTF-1に対するLineage-specific dependencyに関する検討(Lineage-specific dependency of lung adenocarcinomas on the lung development regulator TTF-1)

柳澤聖, 田中寿明, 新城恵子, 田口歩, 前野健, 冨田秀太, 長田啓隆, 高坂貴行, 光冨徹哉, 関戸好孝, 谷本光音, 谷田部恭, 高橋隆

日本癌学会総会記事 66回 417 - 417 2007.8

肺癌において違った形で発現されるマイクロRNAのin silicoスクリーニング(In silico screening of differentially expressed microRNAs in lung cancer)

冨田秀太, 辻河高陽, 松原秀雄, 高橋隆

日本癌学会総会記事 66回 270 - 270 2007.8

Identification of a metastasis signature and the DLX4 homeobox protein as a regulator of metastasis by combined transcriptome approach

S. Tomida, K. Yanagisawa, K. Koshikawa, Y. Yatabe, T. Mitsudomi, H. Osada, T. Takahashi

ONCOGENE 26 ( 31 ) 4600 - 4608 2007.7

Language：English Publisher：NATURE PUBLISHING GROUP

Although widespread metastasis is the major cause of human lung cancer-related deaths, its underlying mechanism remains largely unclear. Our genome-wide comparison of the expression profiles of a highly metastatic lung cancer cell line, NCI-H460-LNM35 (LNM35), and its parental clone, NCI-H460-N15 (N15), resulted in the identification of a cancer metastasis signature composed of 45 genes. Through gene ontology analysis, our study also provided insights into how this 45-gene metastasis signature may contribute to the acquisition of metastatic potential. By applying the signature to datasets of human cancer cases, we could demonstrate significant associations with a subset of cases with poor prognosis not only for the two datasets of cancers of the lung but also for cancers of the breast. Furthermore, we were able to show that enforced expression of the DLX4 homeobox gene, which was identified as a gene with significant downregulation in LNM35 as well as with significant association with favorable prognosis for lung cancer patients, markedly inhibited in vitro motility and invasion as well as in vivo metastasis via both hematogenous and lymphogenous routes. Taken together, these findings indicate that our combined transcriptome analysis is an efficient approach in the search for genes possessing both clinical usefulness in terms of prognostic prediction in human cancer cases and clear functional relevance for studying cancer biology in relation to metastasis.

DOI： 10.1038/sj.onc.1210242

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Lineage-specific dependency of lung adenocarcinomas on the lung development regulator TTF-1

Hisaaki Tanaka, Kiyoshi Yanagisawa, Keiko Shinjo, Ayurnu Taguchi, Ken Maeno, Shuta Tomida, Yukako Shimada, Hirotaka Osada, Takayuki Kosaka, Hideo Matsubara, Tetsuya Mitsudomi, Yoshitaka Sekido, Mitsune Tanimoto, Yasushi Yatabe, Takashi Takahashi

CANCER RESEARCH 67 ( 13 ) 6007 - 6011 2007.7

Language：English Publisher：AMER ASSOC CANCER RESEARCH

Emerging evidence, although currently very sparse, suggests the presence of "lineage-specific dependency" in the survival mechanisms of certain cancers. TTF-1 has a decisive role as a master regulatory transcription factor in lung development and in the maintenance of the functions of terminal respiratory unit (TRU) cells. We show that a subset of lung adenocarcinoma cell lines expressing TTF-1, which presumably represent those derived from the TRU lineage, exhibit marked dependence on the persistent expression of TTF-1. The inhibition of TTF-1 by RNA interference (RNAi) significantly and specifically induced growth inhibition and apoptosis in these adenocarcinoma cell lines. Furthermore, a fraction of TTF-1-expressing tumors and cell lines displayed an increase in the gene dosage of TTF-1 in the analysis of 214 patients with non-small-cell lung cancer, including 174 adenocarcinomas, showing a tendency of higher frequency of increased gene copies at metastatic sites than at primary sites (P = 0.07, by two-sided Fisher's exact test). These findings strongly suggest that in addition to the development and maintenance of TRU lineages in normal lung, sustained TTF-1 expression may be crucial for the survival of a subset of adenocarcinomas that express TTF-1, providing credence for the lineage-specific dependency model.

DOI： 10.1158/0008-5472.CAN-06-4774

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A 25-signal proteomic signature and outcome for patients with resected non-small-cell lung cancer

Kiyoshi Yanagisawa, Shuta Tomida, Yukako Shimada, Yasushi Yatabe, Tetsuya Mitsudomi, Takashi Takahashi

JOURNAL OF THE NATIONAL CANCER INSTITUTE 99 ( 11 ) 858 - 867 2007.6

Language：English Publisher：OXFORD UNIV PRESS INC

Background Among patients with non-small-cell lung cancer (NSCLC), those with poor prognosis cannot be distinguished from those with good prognosis.
Methods Matrix-assisted laser desorption-ionization mass spectrometry was used to analyze protein profiles of 174 specimens from NSCLC tumors and 27 specimens from normal lung tissue and to derive a prognosis-associated proteomic signature. Frozen resected tissue specimens were randomly divided into a training set (116 NSCLC and 20 normal lung specimens) and an independent, blinded validation set (58 NSCLC and seven normal lung specimens). Mass spectrometry signals from training set specimens that were differentially associated with specimens from patients with a high risk of recurrence (i.e., who died within 5 years of surgical treatment because of relapse) compared with those from patients with a low risk of recurrence (i.e., alive with no symptoms of relapse after a median follow-up of 89 months) were selected by use of the Fisher's exact test, the Kruskal-Wallis test, and the significance analysis of microarray test. These signals were used to build an individualized, weighted voting-based prognostic signature. The signature was then validated in the independent dataset. Survival was assessed by multivariable Cox regression analysis. Proteins corresponding to individual signals were identified by ion-trap mass spectrometry coupled with high-performance liquid chromatography. All statistical tests were two-sided.
Results From 2630 mass spectrometry signals from specimens in the training cohort, we derived a signature of 25 signals that was associated with both relapse-free survival and overall survival. Among stage I NSCLC patients in the validation set, the signature was statistically significantly associated with both overall survival (hazard ratio [HR] of death for patients in the high-risk group compared with those in the low-risk group = 61.1, 95% confidence interval [CI] = 8.9 to 419.2, P<.001) and relapse-free survival (HR of relapse = 11.7, 95% CI = 3.1 to 44.8, P<.001). Proteins corresponding to signals in the signature were identified that had various cellular functions, including ribosomal protein L26-like 1, acylphosphatase, and phosphoprotein enriched in astrocytes 15.
Conclusions We defined a mass spectrometry signature that was associated with survival among NSCLC patients and appeared to distinguish those with poor prognosis from those with good prognosis.

DOI： 10.1093/jnci/djk197

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肺癌細胞において過剰発現を示すmiRNAクラスター、miR-17-92の同定と機能解析

林下陽二, 長田啓隆, 立松義郎, 山田英貴, 柳澤聖, 冨田秀太, 谷田部恭, 川原克信, 関戸好孝, 高橋隆

日本癌学会総会記事 65回 157 - 157 2006.9

遺伝子発現プロファイル解析による転移シグネチャーと転移抑制性ホメオボックス遺伝子DLX4の同定

冨田秀太, 柳澤聖, 越川克己, 谷田部恭, 光冨徹哉, 長田啓隆, 高橋隆

日本癌学会総会記事 65回 264 - 264 2006.9

神経内分泌分化誘導因子ASH1によるWntシグナル抑制因子DKK1の発現抑制

長田啓隆, 立松義朗, 竹内俊幸, 冨田秀太, 堀尾芳嗣, 樋田豊明, 谷田部恭, 光冨徹哉, 関戸好孝, 高橋隆

日本癌学会総会記事 65回 64 - 64 2006.9

Expression profile-defined classification of lung adenocarcinoma shows close relationship with underlying major genetic changes and clinicopathologic behaviors

T Takeuchi, S Tomida, Y Yatabe, T Kosaka, H Osada, K Yanagisawa, T Mitsudomi, T Takahashi

JOURNAL OF CLINICAL ONCOLOGY 24 ( 11 ) 1679 - 1688 2006.4

Language：English Publisher：AMER SOC CLINICAL ONCOLOGY

Purpose
This study was conducted to gain insight into the relationship between expression profiles and underlying genetic changes, which are known to be important for the pathogenesis of lung cancers.
Methods
Expression profiles of 18,175 unique genes and three major targets for genetic changes, p53, epidermal growth factor receptor (EGFR, and K-ras, were investigated in 149 patients with non-small-cell lung cancer, including 90 patients with adenocarcinoma to determine their relationships with various clinicopathologic features and Gene Ontology (GO) terms.
Results
This study successfully established a basis for expression profile-defined classification, which can classify adenocarcinomas into two major types, terminal respiratory unit (TRU) type and non-TRU type. Our GO term-based identifier of particular biologic processes, molecular functions, and cellular compartments clearly showed characteristic retention of normal peripheral lung features in TRU type, in sharp contrast to the significant association of non-TRU type with cell cycling and proliferation-related features. While significantly higher frequency of EGFR mutation was observed in TRU type, we found that the presence of EGFR mutations was a significant predictor of shorter postoperative survival for TRU type, independent of disease stage. We were also able to identify a set of genes in vivo with significant upregulation in the presence of EGFR mutations.
Conclusion
This study has shed light on heterogeneity in lung cancers, especially in adenocarcinomas, by establishing a molecularly, genetically, and clinically relevant, expression profile-defined classification. Future studies using independent patient cohorts are warranted to confirm the prognostic significance of EGFR mutations in TRU-type adenocarcinoma.

DOI： 10.1200/JCO.2005.03.8224

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A polycistronic microRNA cluster, miR-17-92, is overexpressed in human lung cancers and enhances cell proliferation

Y Hayashita, H Osada, Y Tatematsu, H Yamada, K Yanagisawa, S Tomida, Y Yatabe, K Kawahara, Y Sekido, T Takahashi

CANCER RESEARCH 65 ( 21 ) 9628 - 9632 2005.11

Language：English Publisher：AMER ASSOC CANCER RESEARCH

MicroRNAs (miRNAs) are small noncoding RNAs, thought to be involved in physiologic and developmental processes by negatively regulating expression of target genes. We have previously reported frequent down-regulation of the let-7 miRNA family in lung cancers and, in the present study, assessed alteration in a panel of 19 lung cancer cell lines. As a result, we found for the first time that the miR-17-92 cluster, which comprises seven miRNAs and resides in intron 3 of the C13orf25 gene at 13q31.3, is markedly overexpressed in lung cancers, especially with small-cell lung cancer histology. Southern blot analysis revealed the presence of increased gene copy numbers of the miRNA cluster in a fraction of lung cancer cell lines with overexpression. In addition, we were able to show predominant localization of C13orf25 transcripts within the nucleus and introduction of the expression construct of the miR-17-92 cluster, but not the putative open reading frame of C13orf25, enhancing lung cancer cell growth. These findings clearly suggest that marked overexpression of the miR-17-92 cluster with occasional gene amplification may play a role in the development of lung cancers, especially in their most aggressive form, small-cell lung cancer, and that the C13orf25 gene may well be serving as a vehicle in this regard.

DOI： 10.1158/0008-5472.CAN-05-2352

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網羅的遺伝子発現プロファイリングによる肺癌の個性の描出

冨田秀太, 竹内俊幸, 谷田部恭, 柳澤聖, 光冨徹哉, 高橋隆

日本癌学会総会記事 64回 402 - 402 2005.9

肺癌におけるDicerの発現低下と外科切除後生存期間の短縮

苅部陽子, 田中寿明, 長田啓隆, 冨田秀太, 立松義朗, 柳澤聖, 谷田部恭, 高見澤潤一, 三好新一郎, 光冨徹哉, 高橋隆

日本癌学会総会記事 64回 389 - 389 2005.9

Reduced expression of Dicer associated with poor prognosis in lung cancer patients

Y Karube, H Tanaka, H Osada, S Tomida, Y Tatematsu, K Yanagisawa, Y Yatabe, J Takamizawa, S Miyoshi, T Mitsudomi, T Takahashi

CANCER SCIENCE 96 ( 2 ) 111 - 115 2005.2

Language：English Publisher：WILEY-BLACKWELL

Emerging evidence suggests that microRNA, which are well-conserved, abundant and small regulatory RNA, may be involved in the pathogenesis of human cancers. We recently reported that expression of let-7 was frequently reduced in lung cancers, and that reduced let-7 expression was significantly associated with shorter patient survival. Two members of the double-stranded RNA-specific endonuclease family, Dicer and Drosha, convert precursor forms of microRNA into their mature forms using a stepwise process. In the present study, we examined expression levels of these genes in 67 non-small cell lung cancer cases, and found for the first time that Dicer expression levels were reduced in a fraction of lung cancers with a significant prognostic impact on the survival of surgically treated cases. It should be noted that multivariate COX regression analysis showed that the prognostic impact of Dicer (P = 0.001) appears to be independent of disease stage (P = 0.001), while logistic regression analysis demonstrated that the higher incidence of reduced Dicer expression in poorly differentiated tumors remained significant even after correction for other parameters (P = 0.02). Given the fundamental and multiple biological roles of Dicer in various cellular processes, our results suggest the involvement of reduced Dicer expression in the development of lung cancers, thus warranting further investigations of the underlying mechanisms, which can be expected to enhance understanding of the molecular pathogenesis of this fatal cancer.

DOI： 10.1111/j.1349-7006.2005.00015.x

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Throwing new light on lung cancer pathogenesis: Updates on three recent topics

S Tomida, Y Yatabe, K Yanagisawa, T Mitsudomi, T Takahashi

CANCER SCIENCE 96 ( 2 ) 63 - 68 2005.2

Language：English Publishing type：Book review, literature introduction, etc. Publisher：WILEY-BLACKWELL

Lung cancers have become the leading cause of cancer deaths in Japan, claiming more than 55 000 lives annually. Unfortunately, substantial improvement in terms of cure rates has not been achieved over the last two decades, although during the same period of time in-depth basic knowledge of the molecular mechanisms, which underlies carcinogenesis and progression of this deadly group of neoplasms, has accumulated at an amazing pace. it has consequently become evident that they have many shared but also distinct features, when comparisons are made not only with other common epithelial cancers of adults, such as colon cancer, but also within the various histologic types of lung cancers themselves. This review article provides an up-date on cutting-edge research into the following three different topics, from which important new insights have been obtained. The first concerns genetic instability, especially chromosome instability, and checkpoint failure in lung cancers. Second, we deal with EGFR mutations, which shows revealing specificities in various aspects. Finally, advances in the expression profiling analysis of both transcriptomes and proteomes of lung cancers are summarized.

DOI： 10.1111/j.1349-7006.2005.00021.x

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Artificial neural network approach for selection of susceptible single nucleotide polymorphisms and construction of prediction model on childhood allergic asthma

Y Tomita, S Tomida, Y Hasegawa, Y Suzuki, T Shirakawa, T Kobayashi, H Honda

BMC BIOINFORMATICS 5 ( 120 ) 2004.9

Language：English Publisher：BIOMED CENTRAL LTD

Background: Screening of various gene markers such as single nucleotide polymorphism ( SNP) and correlation between these markers and development of multifactorial disease have previously been studied. Here, we propose a susceptible marker-selectable artificial neural network ( ANN) for predicting development of allergic disease.
Results: To predict development of childhood allergic asthma (CAA) and select susceptible SNPs, we used an ANN with a parameter decreasing method (PDM) to analyze 25 SNPs of 17 genes in 344 Japanese people, and select 10 susceptible SNPs of CAA. The accuracy of the ANN model with 10 SNPs was 97.7% for learning data and 74.4% for evaluation data. Important combinations were determined by effective combination value (ECV) defined in the present paper. Effective 2-SNP or 3-SNP combinations were found to be concentrated among the 10 selected SNPs.
Conclusion: ANN can reliably select SNP combinations that are associated with CAA. Thus, the ANN can be used to characterize development of complex diseases caused by multiple factors. This is the first report of automatic selection of SNPs related to development of multifactorial disease from SNP data of more than 300 patients.

DOI： 10.1186/1471-2105-5-120

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遺伝子発現プロファイル解析に基づく肺がん患者の予後予測モデルの構築

冨田秀太, 越川克己, 谷田部恭, 原野知子, 小倉信彦, 光冨徹哉, 染真人, 柳澤聖, 高橋利忠, 長田啓隆, 高橋隆

日本癌学会総会記事 63回 452 - 453 2004.9

ヒト肺癌におけるマイクロRNA let-7の発現と各種臨床因子との相関の解析

高見澤潤一, 小西裕之, 柳澤聖, 冨田秀太, 長田啓隆, 遠藤秀紀, 原野知子, 谷田部恭, 梛野正人, 二村雄次, 光冨徹哉, 高橋隆

日本癌学会総会記事 63回 404 - 405 2004.9

高転移性ヒト肺癌細胞亜株(LNM35)における,遺伝子・蛋白の発現プロファイル解析による転移関連因子の探求

柳澤聖, 小西裕之, 冨田秀太, 谷田部恭, 光冨徹哉, 長田啓隆, 高橋隆

日本癌学会総会記事 63回 452 - 452 2004.9

Reduced expression of the let-7 microRNAs in human lung cancers in association with shortened postoperative survival

J Takamizawa, H Konishi, K Yanagisawa, S Tomida, H Osada, H Endoh, T Harano, Y Yatabe, M Nagino, Y Nimura, T Mitsudomi, T Takahashi

CANCER RESEARCH 64 ( 11 ) 3753 - 3756 2004.6

Language：English Publisher：AMER ASSOC CANCER RESEARCH

In this study, we report for the first time reduced expression of the let-7 microRNA in human lung cancers. Interestingly, 143 lung cancer cases that had undergone potentially curative resection could be classified into two major groups according to let-7 expression in unsupervised hierarchical analysis, showing significantly shorter survival after potentially curative resection in cases with reduced let-7 expression (P = 0.0003). Multivariate COX regression analysis showed this prognostic impact to be independent of disease stage (hazard ratio = 2.17; P = 0.009). In addition, overexpression of let-7 in A549 lung adenocarcinoma cell line inhibited lung cancer cell growth in vitro. This study represents the first report of reduced expression of let-7 and the potential clinical and biological effects of such a microRNA alteration.

DOI： 10.1158/0008-5472.CAN-04-0637

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Prognostic model of pulmonary adenocarcinoma by expression profiling of eight genes as determined by quantitative real-time reverse transcriptase polymerase chain reaction

H Endoh, S Tomida, Y Yatabe, H Konishi, H Osada, K Tajima, T Kuwano, T Takahashi, T Mitsudomi

JOURNAL OF CLINICAL ONCOLOGY 22 ( 5 ) 811 - 819 2004.3

Language：English Publisher：AMER SOC CLINICAL ONCOLOGY

Purpose Recently, several expression-profiling experiments have shown that adenocarcinoma can be classified into subgroups that also reflect patient survival. In this study, we examined the expression patterns of 44 genes selected by these studies to test whether their expression patterns were relevant to prognosis in our cohort as well, and to create a prognostic model applicable to clinical practice,
Patients and Methods Expression levels were determined in 85 adenocarcinoma patients by quantitative reverse transcriptase polymerase chain reaction. Cluster analysis was performed, and a prognostic model was created by the proportional hazards model using a stepwise method.
Results Hierarchical clustering divided the cases into three major groups, and group B, comprising 21 cases, had significantly poor survival (P = .0297). Next, we tried to identify a smaller number of genes of particular predictive value, and eight genes (PTK7, CIT, SCNN1A, PGES, ERO1L, ZWINT, and two ESTs) were selected. We then calculated a risk index that was defined as a linear combination of gene expression values weighted by their estimated regression coefficients. The risk index was a significant independent prognostic factor (P = .0021) by multivariate analysis. Furthermore, the robustness of this model was confirmed using an independent set of 21 patients (P = .0085).
Conclusion By analyzing a reasonably small number of genes, patients with adenocarcinoma could be stratified according to their prognosis. The prognostic model could be applicable to future decisions concerning treatment.
(C) 2004 by American Society of Clinical Oncology.

DOI： 10.1200/JCO.2004.04.109

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cDNAマイクロアレイによって選択された44個の遺伝子の発現解析による肺腺癌患者の予後予測モデル

遠藤秀紀, 冨田秀太, 谷田部恭, 小西裕之, 長田啓隆, 田嶋公平, 桑野博行, 高橋隆, 光冨徹哉

日本癌学会総会記事 62回 502 - 502 2003.8

cDNAマイクロアレイによって選択された44個の遺伝子の発現解析による肺腺癌患者の予後予測モデル

遠藤秀紀, 谷田部恭, 冨田秀太, 桑野博行, 高橋隆, 光冨徹哉

日本外科学会雑誌 104 ( 0 ) 258 - 258 2003.4

Analysis of expression profile using fuzzy adaptive resonance theory

S Tomida, T Hanai, H Honda, T Kobayashi

BIOINFORMATICS 18 ( 8 ) 1073 - 1083 2002.8

Language：English Publisher：OXFORD UNIV PRESS

Motivation: It is well understood that the successful clustering of expression profiles give beneficial ideas to understand the functions of uncharacterized genes. In order to realize such a successful clustering, we investigate a clustering method based on adaptive resonance theory (ART) in this report.
Results: We apply Fuzzy ART as a clustering method for analyzing the time series expression data during sporulation of Saccharomyces cerevisiae. The clustering result by Fuzzy ART was compared with those by other clustering methods such as hierarchical clustering, k-means algorithm and self-organizing maps (SOMs). In terms of the mathematical validations, Fuzzy ART achieved the most reasonable clustering. We also verified the robustness of Fuzzy ART using noised data. Furthermore, we defined the correctness ratio of clustering, which is based on genes whose temporal expressions are characterized biologically. Using this definition, it was proved that the clustering ability of Fuzzy ART was superior to other clustering methods such as hierarchical clustering, k-means algorithm and SOMs. Finally, we validate the clustering results by Fuzzy ART in terms of biological functions and evidence.

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Construction of COD simulation model for activated sludge process by recursive fuzzy neural network

S Tomida, T Hanai, H Honda, T Kobayashi

JOURNAL OF CHEMICAL ENGINEERING OF JAPAN 34 ( 3 ) 369 - 375 2001.3

Language：English Publisher：SOC CHEMICAL ENG JAPAN

Using a fuzzy neural network (FNN), we constructed a simulation model which estimates the effluent chemical oxygen demand (COD) value from daily routine measurements. Since the water quality of wastewater is changing day by day, an FNN model with a recursively renewing method of learning data (R-FNN) is proposed. With this R-FNN, Learning data used to construct an FNN model are renewed with elapsed time so as to estimate the effluent COD value with good accuracy. The estimation results for 9 weeks data using R-FNN were compared with those using a conventional FNN. The average error using the R-FNN model was 0.36 mg/l, while that using the conventional FNN was 1.50 mg/l. Moreover, estimation of the effluent COD throughout one year was carried out, and the average error was only 0.40 mg/l. This result can show the usefulness of the R-FNN for the simulation model of the activated sludge process.

DOI： 10.1252/jcej.34.369

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Construction of COD simulation model for activated sludge process by fuzzy neural network

S Tomida, T Hanai, N Ueda, H Honda, T Kobayashi

JOURNAL OF BIOSCIENCE AND BIOENGINEERING 88 ( 2 ) 215 - 220 1999.8

Language：English Publisher：SOC BIOSCIENCE BIOENGINEERING JAPAN

Fuzzy neural network (FNN) was applied to construct a simulation model for estimating the effluent chemical oxygen demand (COD) value of an activated sludge process in a "U" plant, in which most of process variables were measured once an hour. The constructed FNN model could simulate periodic changes in COD with high accuracy. Comparing the simulation result obtained using the FNN model with that obtained using the multiple regression analysis (MRA) model, it was found that the FNN model had 3.7 times higher accuracy than the MRA model. The FNN models corresponding to each of the four seasons were also constructed. Analyzing the fuzzy rules acquired from the FNN models after learning, the operational characteristic of this plant could be elucidated. Construction of the simulation model for another plant "A", in which process variables were measured once a day, was also carried out. This FNN model also had a relatively high accuracy.

DOI： 10.1016/S1389-1723(99)80205-9

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