Faculty Profiles - TOYOOKA Shinichi

Papers - TOYOOKA Shinichi

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非小細胞肺癌II/IIIA期における術後CBDCA+S-1とS-1維持の忍容性試験SLCG1001 長期予後と分子マーカーの解析

吉岡弘鎮, 尾瀬功, 奥村典仁, 園部誠, 中村廣繁, 岡部和倫, 片岡正文, 山下素弘, 中田昌男, 片岡和彦, 山下芳典, 沖田千佳, 能登原憲司, 宗淳一, 堀田勝幸, 松尾恵太郎, 坂本純一, 山本寛斉, 豊岡伸一, 伊達洋至

肺癌 59 ( 6 ) 747 - 747 2019.11

人生100年時代の肺がん治療外科医の立場から

宗淳一, 富沢健二, 武本智樹, 小原秀太, 藤野智大, 古賀教将, 西野将矢, 濱田顕, 千葉眞人, 須田健一, 杉本誠一郎, 豊岡伸一, 光冨徹哉

肺癌 59 ( 6 ) 853 - 853 2019.11

肺門部浸潤肺癌手術例の検討多施設共同データ結果

山下素弘, 豊岡伸一, 伊達洋至, 奥村仁典, 中村宏繁, 岡部和倫, 牧祐歩, 宗淳一

肺癌 59 ( 6 ) 742 - 742 2019.11

ゲフィチニブを用いた化学療法の効果を比較した第III相試験WJTOG3405の全生存期間に関する最終解析(Final overall survival results of WJTOG3405, a phase III trial comparing gefitinib with chemotherapy)

Yoshioka Hiroshige, Shimokawa Mototsugu, Seto Takashi, Morita Satoshi, Yatabe Yasushi, Okamoto Isamu, Tsurutani Junji, Satouchi Miyako, Hirashima Tomonori, Atagi Shinji, Shibata Kazuhiko, Saito Hiroshi, Toyooka Shinichi, Yamamoto Nobuyuki, Nakagawa Kazuhiko, Mitsudomi Tetsuya

肺癌 59 ( 6 ) 629 - 629 2019.11

SPECT/CTを用いて切除範囲を評価した左肺底動脈大動脈起始症の1例

山本諒, 杉本誠一郎, 中田憲太郎, 塩谷俊雄, 三好健太郎, 大谷真二, 山本寛斉, 岡崎幹生, 山根正修, 大藤剛宏, 豊岡伸一, 末澤孝徳

肺癌 59 ( 5 ) 509 - 509 2019.10

新規臨床試験最新情報完全切除非扁平上皮非小細胞肺癌に対する術後補助化学療法第III相試験 JIPANG試験

上野剛, 釼持広知, 山本信之, 山中竹春, 杉尾賢二, 瀬戸貴司, 豊岡伸一, 伊達洋至, 光冨徹哉, 岡本勇, 横井香平, 坂英雄, 岡本浩明, 滝口裕一, 坪井正博

日本癌治療学会学術集会抄録集 57回 SSY14 - 2 2019.10

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

Correction to: Risk assessments for broncho-pleural fistula and respiratory failure after lung cancer surgery by National Clinical Database Japan. Reviewed

Endo S, Ikeda N, Kondo T, Nakajima J, Kondo H, Shimada Y, Sato M, Toyooka S, Okada Y, Sato Y, Yoshino I, Okada M, Okumura M, Chida M, Fukuchi E, Miyata H

General thoracic and cardiovascular surgery 67 ( 10 ) 904 - 906 2019.10

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

ネラチニブ耐性乳がんにおけるYES1の重要性(The importance of YES1 in neratinib-resistant breast cancer)

武田達明, 山本寛斉, 諏澤憲, 北村佳久, 千堂年昭, 豊岡伸一

日本癌学会総会記事 78回 P - 3157 2019.9

ドナー胸腔内所見により再斡旋によるレシピエント変更後に肺移植を行った1例

松原慧, 大谷真二, 山本治慎, 塩谷俊雄, 難波圭, 二萬英斗, 諏澤憲, 三好健太郎, 山本寛斉, 岡崎幹生, 杉本誠一郎, 山根正修, 大藤剛宏, 豊岡伸一

移植 54 ( 総会臨時 ) 315 - 315 2019.9

妊婦に合併した縦隔成熟奇形腫に対して手術を行った1例

宮内俊策, 枝園和彦, 宗淳一, 山本寛斉, 山根正修, 豊岡伸一

日本呼吸器外科学会雑誌 33 ( 6 ) 624 - 628 2019.9

Language：Japanese Publisher：(NPO)日本呼吸器外科学会

縦隔成熟奇形腫は無症状で検診発見されることが多いが、時に急速に増大することがある。今回我々は、妊婦に合併し急速に増大したため妊娠中に手術を施行した症例を経験した。症例は27歳、女性。検診で胸部異常陰影を指摘され当科受診となった。初診時、患者は妊娠10週の妊婦であった。胸部X線写真で右上肺野中枢側に8cm大の腫瘤影、単純MRIで前縦隔に10cm大の多房性嚢胞性病変を認め、成熟奇形腫が疑われた。右前胸部痛が出現しており、腫瘍の急速な増大が考えられ手術の方針とした。手術は妊娠15週に胸骨正中切開で縦隔腫瘍摘出術、右肺上葉・心膜合併部分切除術を施行した。腫瘍は成熟奇形腫の診断で未熟成分や悪性所見は認めなかった。術後経過は良好で、妊娠40週で正常分娩に至った。妊娠と急速増大との因果関係は不明であるが、本症例のような場合でも術前検査や手術時期・方法に注意すれば妊娠中でも安全に手術が行えると考える。(著者抄録)

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Other Link： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2019&ichushi_jid=J02256&link_issn=&doc_id=20190920300008&doc_link_id=10.2995%2Fjacsurg.33.624&url=https%3A%2F%2Fdoi.org%2F10.2995%2Fjacsurg.33.624&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

肺移植後移植片慢性機能不全の予防と治療-本邦における肺移植開始後20年での現状- 肺移植後移植片慢性機能不全(CLAD)における血中micro-RNA発現量の検討 Reviewed

塩谷俊雄, 杉本誠一郎, 松原慧, 山本治慎, 二萬英斗, 三好健太郎, 大谷真二, 岡崎幹生, 山根正修, 大藤剛宏, 豊岡伸一

移植 54 ( 総会臨時 ) 189 - 189 2019.9

生体・脳死肺移植における予後予測因子としてのPrognostic Nutrition Index(PNI)の有用性 Reviewed

山本治慎, 杉本誠一郎, 塩谷俊雄, 三好健太郎, 大谷真二, 岡崎幹生, 山根正修, 大藤剛宏, 豊岡伸一

移植 54 ( 総会臨時 ) 215 - 215 2019.9

ハイリスク症例に対する肺移植高度の胸膜癒着を認めたレシピエントに対する肺移植 Reviewed

杉本誠一郎, 塩谷俊雄, 山本治慎, 大河知世, 三好健太郎, 大谷真二, 岡崎幹生, 山根正修, 大藤剛宏, 豊岡伸一

移植 54 ( 総会臨時 ) 174 - 174 2019.9

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

バイオバンキングが切り拓く新しいがん研究わが国におけるクリニカルバイオバンクネットワークの構築(Innovative cancer research based on biobanking Clinical biobank network in Japan)

武藤学, 金井雅史, 鶴山竜昭, 松本繁巳, 豊岡伸一, 秋田弘俊, 松原久裕, 西原広史, 末岡榮三朗, 池田貞勝

日本癌学会総会記事 78回 S11 - 4 2019.9

Upregulation of Mobility in Pancreatic Cancer Cells by Secreted S100A11 Through Activation of Surrounding Fibroblasts. Reviewed International journal

Yosuke Mitsui, Nahoko Tomonobu, Masami Watanabe, Rie Kinoshita, I Wayan Sumardika, Chen Youyi, Hitoshi Murata, Ken-Ichi Yamamoto, Takuya Sadahira, Acosta Gonzalez Herik Rodrigo, Hitoshi Takamatsu, Kota Araki, Akira Yamauchi, Masahiro Yamamura, Hideyo Fujiwara, Yusuke Inoue, Junichiro Futami, Ken Saito, Hidekazu Iioka, Eisaku Kondo, Masahiro Nishibori, Shinichi Toyooka, Yasuhiko Yamamoto, Yasutomo Nasu, Masakiyo Sakaguchi

Oncology research 27 ( 8 ) 945 - 956 2019.8

Language：English Publishing type：Research paper (scientific journal)

S100A11, a member of the S100 family of proteins, is actively secreted from pancreatic ductal adenocarcinoma (PDAC) cells. However, the role of the extracellular S100A11 in PDAC progression remains unclear. In the present study, we investigated the extracellular role of S100A11 in crosstalking between PDAC cells and surrounding fibroblasts in PDAC progression. An abundant S100A11 secreted from pancreatic cancer cells stimulated neighboring fibroblasts through receptor for advanced glycation end products (RAGE) upon S100A11 binding and was followed by not only an enhanced cancer cell motility in vitro but also an increased number of the PDAC-derived circulating tumor cells (CTCs) in vivo. Mechanistic investigation of RAGE downstream in fibroblasts revealed a novel contribution of a mitogen-activated protein kinase kinase kinase (MAPKKK), tumor progression locus 2 (TPL2), which is required for positive regulation of PDAC cell motility through induction of cyclooxygenase 2 (COX2) and its catalyzed production of prostaglandin E2 (PGE2), a strong chemoattractive fatty acid. The extracellularly released PGE2 from fibroblasts was required for the rise in cellular migration as well as infiltration of their adjacent PDAC cells in a coculture setting. Taken together, our data reveal a novel role of the secretory S100A11 in PDAC disseminative progression through activation of surrounding fibroblasts triggered by the S100A11-RAGE-TPL2-COX2 pathway. The findings of this study will contribute to the establishment of a novel therapeutic antidote to PDACs that are difficult to treat by regulating cancer-associated fibroblasts (CAFs) through targeting the identified pathway.

DOI： 10.3727/096504019X15555408784978

PubMed

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Impact of chronic lung allograft dysfunction, especially restrictive allograft syndrome, on the survival after living-donor lobar lung transplantation compared with cadaveric lung transplantation in adults: a single-center experience. Reviewed

Seiichiro Sugimoto, Haruchika Yamamoto, Takeshi Kurosaki, Shinji Otani, Mikio Okazaki, Masaomi Yamane, Shinichi Toyooka, Takahiro Oto

Surgery today 49 ( 8 ) 686 - 693 2019.8

Language：English Publishing type：Research paper (scientific journal)

PURPOSE: The differences in chronic lung allograft dysfunction (CLAD) between living-donor lobar lung transplantation (LDLLT) and cadaveric lung transplantation (CLT) remain unclear. We conducted this study to compare the impact of CLAD on the outcomes after LDLLT vs. CLT. METHODS: We conducted a retrospective review of the data of 97 recipients of bilateral lung transplantation, including 51 recipients of LDLLT and 46 recipients of CLT. RESULTS: The CLAD-free survival and overall survival after LDLLT were similar to those after CLT. CLAD and restrictive allograft syndrome (RAS), but not bronchiolitis obliterans syndrome (BOS), developed significantly later after LDLLT than after CLT (p = 0.015 and p = 0.035). Consequently, patients with CLAD and RAS, but not those with BOS, after LDLLT had a significantly better overall survival than those after CLT (p = 0.037 and p = 0.0006). Furthermore, after the diagnosis of CLAD, the survival of patients with RAS after LDLLT tended to be better than that after CLT (p = 0.083). CONCLUSION: CLAD, especially RAS, appears to develop later after LDLLT than after CLT and seems to have a lower impact on the overall survival after LDLLT than that after CLT.

DOI： 10.1007/s00595-019-01782-0

PubMed

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Acquired resistance mechanisms to afatinib in HER2-amplified gastric cancer cells. Reviewed International journal

Takahiro Yoshioka, Kazuhiko Shien, Tatsuaki Takeda, Yuta Takahashi, Eisuke Kurihara, Yusuke Ogoshi, Kei Namba, Hidejiro Torigoe, Hiroki Sato, Shuta Tomida, Hiromasa Yamamoto, Junichi Soh, Toshiyoshi Fujiwara, Shinichi Toyooka

Cancer science 110 ( 8 ) 2549 - 2557 2019.8

Language：English Publishing type：Research paper (scientific journal)

Cancer treatment, especially that for breast and lung cancer, has entered a new era and continues to evolve, with the development of genome analysis technology and the advent of molecular targeted drugs including tyrosine kinase inhibitors. Nevertheless, acquired drug resistance to molecular targeted drugs is unavoidable, creating a clinically challenging problem. We recently reported the antitumor effect of a pan-HER inhibitor, afatinib, against human epidermal growth factor receptor 2 (HER2)-amplified gastric cancer cells. The purpose of the present study was to identify the mechanisms of acquired afatinib resistance and to investigate the treatment strategies for HER2-amplified gastric cancer cells. Two afatinib-resistant gastric cancer cell lines were established from 2 HER2-amplified cell lines, N87 and SNU216. Subsequently, we investigated the molecular profiles of resistant cells. The activation of the HER2 pathway was downregulated in N87-derived resistant cells, whereas it was upregulated in SNU216-derived resistant cells. In the N87-derived cell line, both MET and AXL were activated, and combination treatment with afatinib and cabozantinib, a multikinase inhibitor that inhibits MET and AXL, suppressed the cell growth of cells with acquired resistance both in vitro and in vivo. In the SNU216-derived cell line, YES1, which is a member of the Src family, was remarkably activated, and dasatinib, a Src inhibitor, exerted a strong antitumor effect in these cells. In conclusion, we identified MET and AXL activation in addition to YES1 activation as novel mechanisms of afatinib resistance in HER2-driven gastric cancer. Our results also indicated that treatment strategies targeting individual mechanisms of resistance are key to overcoming such resistance.

DOI： 10.1111/cas.14089

PubMed

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Papers - TOYOOKA Shinichi