Updated on 2024/03/28

写真a

 
NOZAKI Koichiro
 
Organization
University Medical and Dental Hospital Respiratory Medicine and Infectious Disease Assistant Professor
Title
Assistant Professor
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Degree

  • 博士(医学) ( 2015.3 )

Research Interests

  • Resipiratory medicine

  • Lung Cancer

Research Areas

  • Life Science / Tumor diagnostics and therapeutics  / Lung Cancer

Research History (researchmap)

  • 新潟大学医歯学総合病院   呼吸器・感染症内科   病院専任助教

    2018.3

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    Country:Japan

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Research History

  • Niigata University   University Medical and Dental Hospital Respiratory Medicine and Infectious Disease   Assistant Professor

    2020.4

  • Niigata University   University Medical and Dental Hospital Respiratory Medicine and Infectious Disease   Specially Appointed Assistant Professor

    2019.10 - 2020.3

  • Niigata University   University Medical and Dental Hospital Respiratory Medicine and Infectious Disease   Specially Appointed Assistant Professor

    2018.10 - 2019.3

Education

  • Niigata University   新潟大学医歯学総合研究科   生体機能調節医学専攻 内部環境医学講座 呼吸器内科学

    2011.4 - 2014.3

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    Country: Japan

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  • Niigata University   Faculty of Medicine   School of Medicine

    2002.4 - 2008.3

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    Country: Japan

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Professional Memberships

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Papers

  • 免疫チェックポイント阻害薬が著効した肺紡錘細胞癌の2例

    鈴木 遼, 庄子 聡, 藤崎 俊哉, 大坪 亜矢, 野嵜 幸一郎, 田中 知宏, 才田 優, 近藤 利恵, 島 賢治郎, 木村 陽介, 青木 信将, 大嶋 康義, 渡部 聡, 小屋 俊之, 菊地 利明

    肺癌   62 ( 6 )   791 - 791   2022.11

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    Language:Japanese   Publisher:(NPO)日本肺癌学会  

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  • アレクチニブの減感作療法により内服再開が可能であったALK融合遺伝子陽性肺腺癌の1例

    後藤 優佳, 近藤 利恵, 高橋 美帆, 市川 紘将, 田中 知宏, 渡部 聡, 鈴木 遼, 大坪 亜矢, 庄子 聡, 野嵜 幸一郎, 才田 優, 青木 信将, 大嶋 康義, 小屋 俊之, 武居 慎吾, 河合 亨, 結城 明彦, 濱 菜摘, 阿部 理一郎, 菊地 利明

    肺癌   62 ( 6 )   739 - 739   2022.11

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  • 小細胞肺癌に転化したEGFR遺伝子変異陽性肺腺癌に対してABCP療法を行った1例

    野嵜 幸一郎, 後藤 優佳, 鈴木 遼, 大坪 亜矢, 庄子 聡, 田中 知宏, 才田 優, 近藤 利恵, 島 賢治郎, 木村 陽介, 青木 信将, 大嶋 康義, 渡部 聡, 小屋 俊之, 菊地 利明

    肺癌   62 ( 6 )   783 - 783   2022.11

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  • Efficacy and safety of amrubicin therapy after chemoimmunotherapy in small cell lung cancer patients. International journal

    Kohei Kushiro, Satoshi Watanabe, Yuka Goto, Toshiya Fujisaki, Naohiro Yanagimura, Aya Ohtsubo, Satoshi Shoji, Koichiro Nozaki, Tomohiro Tanaka, Yu Saida, Yusuke Sato, Takeshi Ota, Jun Koshio, Yoshiki Hayashi, Takao Miyabayashi, Naoya Matsumoto, Kosuke Ichikawa, Kenichi Koyama, Toshiaki Kikuchi

    Translational lung cancer research   11 ( 9 )   1858 - 1865   2022.9

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    BACKGROUND: Although the addition of immune checkpoint inhibitors (ICIs) to platinum-doublet chemotherapy has improved the efficacy of first-line therapy in extensive-disease small cell lung cancer (SCLC) patients, the best treatment option for patients with recurrent SCLC has not yet been determined. We conducted a retrospective study to evaluate the efficacy and safety of amrubicin (AMR) therapy after treatment with ICIs. METHODS: We retrospectively assessed patients with recurrent SCLC who received AMR after chemoimmunotherapy at the Niigata Lung Cancer Treatment Group from August 2019 to February 2021. RESULTS: This analysis included 30 patients. The median progression-free survival (PFS) and overall survival (OS) were 3.8 (95% CI: 2.7-4.2) and 10 (95% CI: 7.4-14.8) months, respectively. The median PFS and OS did not significantly differ between the sensitive and refractory groups [PFS; 3.1 (95% CI: 1.1-4.0) vs. 4.2 (95% CI: 2.3-4.8) months, P=0.1142, OS; 10.0 (95% CI: 5.2-14.8) vs. 10.4 (95% CI: 3.8-NE) months, P=0.5525]. The most common adverse event was grade ≥3 neutropenia, which occurred in 22 of 30 patients (73%), and 2 patients (7%) discontinued AMR due to adverse events. CONCLUSIONS: AMR after chemoimmunotherapy shows good clinical efficacy and safety in patients with recurrent SCLC.

    DOI: 10.21037/tlcr-22-225

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  • Phase II study of nanoparticle albumin-bound paclitaxel monotherapy for relapsed non-small cell lung cancer with patient-reported outcomes (NLCTG1302). International journal

    Satoshi Shoji, Satoru Miura, Satoshi Watanabe, Aya Ohtsubo, Koichiro Nozaki, Yu Saida, Kosuke Ichikawa, Rie Kondo, Tomohiro Tanaka, Kenichi Koyama, Hiroshi Tanaka, Masaaki Okajima, Tetsuya Abe, Takeshi Ota, Takashi Ishida, Masato Makino, Akira Iwashima, Kazuhiro Sato, Naoya Matsumoto, Hirohisa Yoshizawa, Toshiaki Kikuchi

    Translational lung cancer research   11 ( 7 )   1359 - 1368   2022.7

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    BACKGROUND: This multicenter, open-label, single-arm phase II study [Niigata Lung Cancer Treatment Group (NLCTG) 1302] was conducted to evaluate the efficacy and safety of nanoparticle albumin-bound paclitaxel (nab-paclitaxel) monotherapy for previously treated patients with advanced non-small cell lung cancer (NSCLC). We also investigated chemotherapy-induced peripheral neuropathy (CIPN) to evaluate the quality of life (QOL). METHODS: Sixty-five patients with advanced NSCLC from 14 participating institutions who had previously undergone one or two cytotoxic chemotherapy regimens were enrolled in this study. The patients received 100 mg/m2 nab-paclitaxel intravenously on days 1, 8, and 15, every 4 weeks. The primary endpoint was overall objective response rate. CIPN symptoms were prospectively assessed using the Patient Neurotoxicity Questionnaire (PNQ) and Common Terminology Criteria for Adverse Events (CTCAE). RESULTS: The overall response rate (ORR) was 18.5% [95% confidence interval (CI): 10.9-29.6%], and the median progression-free survival (PFS) was 3.4 (95% CI: 2.5-4.3) months. Median overall survival (OS) was 8.6 (95% CI: 7.1-10.2) months. The most common non-hematologic grade ≥3 adverse events were infection (7.7%) and hyponatremia (4.6%). Neutropenia was the most common grade 3 or 4 adverse event (30.8%), and febrile neutropenia developed in 6.2% patients. The PNQ and CTCAE scores for motor peripheral neuropathy were low (kappa =0.10). CONCLUSIONS: The primary endpoint was achieved. Nab-paclitaxel was well tolerated and showed anti-tumor activity in patients with previously treated NSCLC. This study demonstrates a low degree of concordance in CIPN grading between physicians and patients. TRIAL REGISTRATION: University hospital Medical Information Network Clinical Trial Registry (ID: UMIN000012343).

    DOI: 10.21037/tlcr-22-89

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  • Observational study of rebiopsy in EGFR-TKI-resistant patients with EGFR mutation-positive advanced NSCLC. International journal

    Kenichi Koyama, Satoru Miura, Satoshi Watanabe, Satoshi Shoji, Jun Koshio, Yoshiki Hayashi, Daisuke Ishikawa, Ko Sato, Takao Miyabayashi, Masaaki Okajima, Takeshi Ota, Tomohiro Tanaka, Naoya Matsumoto, Hideyuki Kuriyama, Tetsuya Abe, Koichiro Nozaki, Kosuke Ichikawa, Rie Kondo, Hiroshi Tanaka, Toshiaki Kikuchi

    Scientific reports   12 ( 1 )   6367 - 6367   2022.4

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    The identification of acquired resistance mutations has been essential in non-small-cell lung cancer (NSCLC) patients with epidermal growth factor receptor (EGFR) active mutations. Rebiopsy plays a pivotal role in selecting the optimal treatment for patients who develop resistance to initial EGFR-tyrosine kinase inhibitors (EGFR-TKIs). This multicenter, observational study was conducted to investigate the details of rebiopsy in Japanese clinical practice. The primary endpoints were the implementation rate of rebiopsy and the concordance rate for T790M mutation detection between histological and cytological specimens using the cobas EGFR Mutation Test, version 2. One hundred ninety-four patients with EGFR-mutant NSCLC were enrolled, and 120 patients developed acquired resistance to EGFR-TKIs. The median age was 68 years (range 20-87), and 52.5% of the patients were women. Rebiopsy was performed in 109 patients, and the implementation rate of rebiopsy was 90.8%. The success rates of rebiopsy in the total, histology, cytology and liquid biopsy populations were 67.9%, 81.3%, 66.7% and 43.8%, respectively. The positive percent agreement and the negative percent agreement in the detection of the T790M mutation between the histological and cytological specimens were both 90.9%. Obtaining histological or cytological tissue samples at rebiopsy may contribute to improving the detection rate of the T790M mutation (trial registration number: UMIN000026019).

    DOI: 10.1038/s41598-022-10288-8

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  • Prognostic significance of procalcitonin in small cell lung cancer

    Kosuke Ichikawa, Satoshi Watanabe, Satoru Miura, Aya Ohtsubo, Satoshi Shoji, Koichiro Nozaki, Tomohiro Tanaka, Yu Saida, Rie Kondo, Satoshi Hokari, Nobumasa Aoki, Yasuyoshi Ohshima, Toshiyuki Koya, Toshiaki Kikuchi

    Translational Lung Cancer Research   11 ( 1 )   43 - 52   2022.1

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    DOI: 10.21037/tlcr-21-838

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  • Effectiveness of afatinib in an NSCLC patient with EGFR mutation and early progression to osimertinib: a case report. International journal

    Koichiro Nozaki, Satoshi Watanabe, Kazuto Nishio, Kazuko Sakai, Toshiaki Kikuchi

    Translational cancer research   11 ( 1 )   295 - 298   2022.1

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    Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), shows great clinical activity in non-small cell lung cancer (NSCLC) patients with EGFR mutations regardless of T790M mutation at first-line chemotherapy. Previous studies demonstrated that there are few patients with initial resistance to osimertinib. Here, we describe a case to report the efficacy of afatinib in an EGFR-mutated NSCLC patient with early progression to first-line osimertinib treatment. A 68-year-old Japanese male was diagnosed with stage IVB lung adenocarcinoma with the EGFR L858R mutation in exon 21. Two months after the start of osimertinib, his tumor progressed at the initial response evaluation. Because he refused to receive cytotoxic chemotherapy, afatinib treatment was initiated. He was administered afatinib, and the tumor shrank. After five months of afatinib treatment, nevertheless the primary tumor was not enlarged, he experienced disease progression with leptomeningeal metastasis and passed away. To elucidate the resistance mechanisms of osimertinib in this patient, we performed next-generation sequencing (NGS) on tumor samples from pleural effusions after osimertinib failure. NGS revealed no specific gene mutations causing resistance to osimertinib except for the EGFR L858R mutation; however, his tumor had a relatively high tumor mutational burden. Afatinib is considered an option for EGFR-mutated patients with early progression to osimertinib.

    DOI: 10.21037/tcr-21-1850

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  • Nivolumab+ipilimumab併用療法が奏効した肺原発紡錘細胞癌の一例

    有田 将史, 倉科 健司, 原山 幸代, 大坪 亜矢, 庄子 聡, 田中 知宏, 野嵜 幸一郎, 才田 優, 大嶋 康義, 渡部 聡, 小屋 俊之, 佐藤 英夫, 菊地 利明

    肺癌   61 ( 6 )   698 - 698   2021.10

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  • 非小細胞肺癌に対するアテゾリズマブ/カルボプラチン/パクリタキセル/ベバシズマブ療法の後方視的解析

    庄子 聡, 渡部 聡, 大坪 亜矢, 野嵜 幸一郎, 田中 知宏, 才田 優, 近藤 利恵, 木村 陽介, 青木 信将, 大嶋 康義, 小屋 俊之, 菊地 利明

    肺癌   61 ( 6 )   696 - 696   2021.10

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  • The Prognostic Significance of the Continuous Administration of Anti-PD-1 Antibody via Continuation or Rechallenge After the Occurrence of Immune-Related Adverse Events

    Toshiya Fujisaki, Satoshi Watanabe, Takeshi Ota, Kohei Kushiro, Yusuke Sato, Miho Takahashi, Aya Ohtsubo, Satoshi Shoji, Koichiro Nozaki, Kosuke Ichikawa, Satoshi Hokari, Rie Kondo, Takao Miyabayashi, Tetsuya Abe, Satoru Miura, Hiroshi Tanaka, Masaaki Okajima, Masaki Terada, Naoya Matsumoto, Takashi Ishida, Akira Iwashima, Kazuhiro Sato, Hirohisa Yoshizawa, Nobumasa Aoki, Masachika Hayashi, Yasuyoshi Ohshima, Toshiyuki Koya, Toshiaki Kikuchi

    Frontiers in Oncology   11   2021.9

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    <sec><title>Objectives</title>Although immune checkpoint inhibitors (ICIs) have been shown to improve overall survival (OS) in advanced non-small-cell lung cancer (NSCLC) patients, ICIs sometimes cause various types of immune-related adverse events (irAEs), which lead to the interruption of ICI treatment. This study aims to evaluate the clinical significance of the continuation of ICIs in NSCLC patients with irAEs and to assess the safety and efficacy of the readministration of ICIs after their discontinuation due to irAEs.

    </sec><sec><title>Methods</title>We retrospectively identified patients with advanced NSCLC who were treated with first- to third-line anti-programmed cell death-1 (PD-1) therapy from January 2016 through October 2017 at multiple institutions belonging to the Niigata Lung Cancer Treatment Group. Progression-free survival (PFS) and OS from the initiation of ICI treatment were analyzed in patients with and without irAEs, with and without ICI interruption, and with and without ICI readministration. A 6-week landmark analysis of PFS and OS was performed to minimize the lead-time bias associated with time-dependent factors.

    </sec><sec><title>Results</title>Of 231 patients who received anti-PD-1 antibodies, 93 patients (40%) developed irAEs. Of 84 eligible patients with irAEs, 32 patients (14%) continued ICIs, and OS was significantly longer in patients who continued ICIs than that in patients who discontinued ICIs [not reached (95% CI: NE-NE) <italic>vs</italic>. not reached (95% CI: 22.4–NE); p = 0.025]. Of 52 patients who discontinued ICIs, 14 patients (6.1%) readministered ICIs, and OS in patients with ICI readministration was significantly longer than that in patients without ICI readministration [not reached (95% CI: NE-NE) <italic>vs</italic>. not reached (95% CI: 8.4–NE); p = 0.031].

    </sec><sec><title>Conclusion</title>The current study demonstrated that both the continuation and readministration of ICIs after irAE occurrence improved OS compared to the permanent interruption of ICIs in NSCLC patients with ICI-related irAEs.

    </sec>

    DOI: 10.3389/fonc.2021.704475

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  • ニンテダニブは腫瘍微小環境を改善することでPD-1阻害剤の抗腫瘍効果を増強する

    鈴木 遼, 渡部 聡, 久代 航平, 関谷 友樹, 藤崎 俊哉, 安部 悠子, 佐藤 美由紀, 大坪 亜矢, 庄子 聡, 田中 知宏, 野嵜 幸一郎, 才田 優, 穂苅 諭, 大嶋 康義, 小屋 俊之, 菊地 利明

    日本癌学会総会記事   80回   [J12 - 6]   2021.9

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  • Subsequent systemic therapy for non-small cell lung cancer patients with immune checkpoint inhibitor-related interstitial lung disease. International journal

    Yusuke Sato, Satoshi Watanabe, Takeshi Ota, Kohei Kushiro, Toshiya Fujisaki, Miho Takahashi, Aya Ohtsubo, Satoshi Shoji, Koichiro Nozaki, Kosuke Ichikawa, Satoshi Hokari, Rie Kondo, Masachika Hayashi, Hiroyuki Ishikawa, Takao Miyabayashi, Tetsuya Abe, Satoru Miura, Hiroshi Tanaka, Masaaki Okajima, Masaki Terada, Takashi Ishida, Akira Iwashima, Kazuhiro Sato, Hirohisa Yoshizawa, Nobumasa Aoki, Yasuyoshi Ohshima, Toshiyuki Koya, Toshiaki Kikuchi

    Translational lung cancer research   10 ( 7 )   3132 - 3143   2021.7

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    Background: Although immune checkpoint inhibitors (ICIs) are effective for advanced non-small cell lung cancer (NSCLC), ICIs may cause interstitial lung disease (ILD), which results in treatment discontinuation and is sometimes fatal. Despite the high incidence of ICI-related ILD, there are few cancer treatment options for patients. This study aimed to evaluate the safety and efficacy of subsequent systemic cancer therapy in NSCLC patients with ICI-related ILD. Methods: We retrospectively assessed NSCLC patients who received programmed cell death-1 (PD-1) inhibitors as first- to third-line therapy at participating institutions of the Niigata Lung Cancer Treatment Group from January 2016 to October 2017. Results: This analysis included 231 patients, 32 (14%) of whom developed ICI-related ILD. Of these patients, 16 (7%) received subsequent systemic cancer treatments. The median overall survival (OS) tended to be longer in the systemic cancer therapy group than in the no systemic cancer therapy group [22.2 months (95% CI: 1-NE) vs. 4.5 months (95% CI: 1-NE); P=0.067]. ICI-related ILD recurred in half of the patients who received systemic cancer therapy, and the median OS tended to be shorter in patients with recurrent ICI-related ILD [22.0 months (95% CI: 1-NE) vs. 7.0 months (95% CI: 1-NE); P=0.3154]. Conclusions: According to the current study, systemic cancer treatment is effective in patients with ICI-related ILD; however, its safety is uncertain because of the high risk of ICI-related ILD recurrence and poor survival outcome following ILD recurrence.

    DOI: 10.21037/tlcr-21-198

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  • Combination therapy of cisplatin with cilastatin enables an increased dose of cisplatin, enhancing its antitumor effect by suppression of nephrotoxicity. International journal

    Masashi Arita, Satoshi Watanabe, Nobumasa Aoki, Shoji Kuwahara, Ryo Suzuki, Sawako Goto, Yuko Abe, Miho Takahashi, Miyuki Sato, Satoshi Hokari, Aya Ohtsubo, Satoshi Shoji, Koichiro Nozaki, Kosuke Ichikawa, Rie Kondo, Masachika Hayashi, Yasuyoshi Ohshima, Hideyuki Kabasawa, Michihiro Hosojima, Toshiyuki Koya, Akihiko Saito, Toshiaki Kikuchi

    Scientific reports   11 ( 1 )   750 - 750   2021.1

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    Cisplatin, one of the most active anticancer agents, is widely used in standard chemotherapy for various cancers. Cisplatin is more poorly tolerated than other chemotherapeutic drugs, and the main dose-limiting toxicity of cisplatin is its nephrotoxicity, which is dose-dependent. Although less toxic methods of cisplatin administration have been established, cisplatin-induced nephrotoxicity remains an unsolved problem. Megalin is an endocytic receptor expressed at the apical membrane of proximal tubules. We previously demonstrated that nephrotoxic drugs, including cisplatin, are reabsorbed through megalin and cause proximal tubular cell injury. We further found that cilastatin blocked the binding of cisplatin to megalin in vitro. In this study, we investigated whether cilastatin could reduce cisplatin-induced nephrotoxicity without influencing the antitumor effects of cisplatin. Nephrotoxicity was decreased or absent in mice treated with cisplatin and cilastatin, as determined by kidney injury molecule-1 staining and the blood urea nitrogen content. Combined with cilastatin, a twofold dose of cisplatin was used to successfully treat the mice, which enhanced the antitumor effects of cisplatin but reduced its nephrotoxicity. These findings suggest that we can increase the dose of cisplatin when combined with cilastatin and improve the outcome of cancer patients.

    DOI: 10.1038/s41598-020-80853-6

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  • ニンテダニブはMDSCを抑制することでPD-1阻害剤の抗腫瘍効果を増強する

    鈴木 遼, 渡部 聡, 有田 将史, 関谷 友樹, 安部 悠子, 佐藤 美由紀, 高橋 美帆, 大坪 亜矢, 庄子 聡, 野嵜 幸一郎, 市川 紘将, 穂苅 諭, 近藤 利恵, 大嶋 康義, 小屋 俊之, 菊地 利明

    日本癌学会総会記事   79回   PJ12 - 9   2020.10

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  • シェーグレン症候群を有する非小細胞肺癌に対して免疫チェックポイント阻害薬を安全に使用できた一例

    大坪 亜矢, 久代 航平, 佐藤 佑輔, 高橋 美帆, 庄子 聡, 野嵜 幸一郎, 穂苅 諭, 市川 紘将, 近藤 利恵, 青木 信将, 大嶋 康義, 林 正周, 渡部 聡, 小屋 俊之, 菊地 利明

    肺癌   60 ( 6 )   724 - 724   2020.10

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  • ペムブロリズマブによる大腸炎発症後、再投与で小腸炎を発症した非小細胞肺癌の一例

    庄子 聡, 高橋 美帆, 大坪 亜矢, 野嵜 幸一郎, 市川 紘将, 近藤 利恵, 青木 信将, 大嶋 康義, 林 正周, 渡部 聡, 小屋 俊之, 近藤 修平, 梅津 哉, 菊地 利明

    肺癌   60 ( 6 )   769 - 769   2020.10

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  • Prognostic significance of the radiologic features of pneumonitis induced by anti-PD-1 therapy. International journal

    Satoshi Watanabe, Takeshi Ota, Masachika Hayashi, Hiroyuki Ishikawa, Aya Otsubo, Satoshi Shoji, Koichiro Nozaki, Kosuke Ichikawa, Rie Kondo, Takao Miyabayashi, Satoru Miura, Hiroshi Tanaka, Tetsuya Abe, Masaaki Okajima, Masaki Terada, Takashi Ishida, Akira Iwashima, Kazuhiro Sato, Hirohisa Yoshizawa, Toshiaki Kikuchi

    Cancer medicine   9 ( 9 )   3070 - 3077   2020.5

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    BACKGROUND: Interstitial lung disease (ILD) induced by anti-programmed-cell death-1 (PD-1) and anti-PD-ligand 1 (PD-L1) is potentially life-threatening and is a common reason of the discontinuation of therapy. In contrast, an enhancement in antitumor effects was reported in patients who developed immune-related adverse events, including ILD. Although recent evidence suggests that radiologic patterns of ILD may reflect the severity of ILD and the antitumor immune responses to anti-PD-1/PD-L1 therapies, the association between radiologic features and clinical outcomes remains unclear. METHODS: Patients with advanced non-small-cell lung cancer who were treated with 1st to 3rd line anti-PD-1 therapy from January 2016 through October 2017 were identified at multiple institutions belonging to the Niigata Lung Cancer Treatment Group. ILD was diagnosed by the treating physicians, and chest computed tomography scans were independently reviewed to assess the radiologic features of ILD. RESULTS: A total of 231 patients who received anti-PD-1 therapy were enrolled. Thirty-one patients (14%) developed ILD. Sixteen patients were classified as having ground glass opacities (GGO), 16 were classified as having cryptogenic organizing pneumonia (COP), and one was classified as having pneumonitis not otherwise specified. Patients with GGO had significantly worse overall survival time compared to patients with COP (7.8 months (95% CI: 2.2-NE) versus not reached (95% CI: 13.2-NE); P = 0.0175). Multivariate analysis of all 231 patients also revealed that PS = 1 and ≥2 and GGO were significant predictors of a worse overall survival. CONCLUSIONS: This study demonstrated that patients who developed GGO exhibited worse outcomes among non-small-cell lung cancer patients receiving anti-PD-1 therapies.

    DOI: 10.1002/cam4.2974

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  • CBDCA+Pemetrexed+Pembrolizumabが奏効したTrousseau症候群合併肺腺癌の一例

    野嵜 幸一郎, 島津 翔, 尾形 英至, 吉澤 和孝, 近藤 利恵, 木村 陽介, 青木 信将, 渡部 聡, 大嶋 康義, 庄子 聡, 大坪 亜矢, 市川 紘将, 菊地 利明

    肺癌   59 ( 6 )   814 - 814   2019.11

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  • Efficacy of EGFR-TKIs with or without upfront brain radiotherapy for EGFR-mutant NSCLC patients with central nervous system metastases. International journal

    Yu Saida, Satoshi Watanabe, Tetsuya Abe, Satoshi Shoji, Koichiro Nozaki, Kosuke Ichikawa, Rie Kondo, Kenichi Koyama, Satoru Miura, Hiroshi Tanaka, Masaaki Okajima, Masaki Terada, Takashi Ishida, Hiroki Tsukada, Masato Makino, Akira Iwashima, Kazuhiro Sato, Naoya Matsumoto, Hirohisa Yoshizawa, Toshiaki Kikuchi

    Thoracic cancer   10 ( 11 )   2106 - 2116   2019.11

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    BACKGROUND: Although the clinical efficacy of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in EGFR-mutant non-small cell lung cancer (NSCLC) patients has been demonstrated, their efficacy in EGFR-mutant NSCLCs with central nervous system (CNS) metastases and the role of radiotherapy remain unclear. This study aimed to determine if it is preferable to add upfront cranial radiotherapy to EGFR-TKIs in patients with EGFR-mutant NSCLC with newly diagnosed brain metastases. METHODS: We retrospectively analyzed the data of EGFR-mutant NSCLC patients with CNS metastases who received EGFR-TKIs as a first-line therapy. RESULTS: A total of 104 patients were enrolled and 39 patients received upfront brain radiotherapy, while 65 patients received first and second generation EGFR-TKIs first. The median time to treatment failure (TTF) was 7.8 months (95% confidence interval [CI]: 6.3-9.4). The median survival time (MST) was 24.0 months (95% CI: 20.1-30.1). The overall response rate of the CNS was 37%. The median CNS progression-free survival (PFS) was 13.2 months (95% CI: 10.0-16.2). Brain radiotherapy prior to EGFR-TKI prolonged TTF (11.2 vs. 6.8 months, P = 0.038) and tended to prolong CNS-PFS (15.6 vs. 11.1 months, P = 0.096) but was not significantly associated with overall survival (MST 26.1 vs. 24.0 months, P = 0.525). Univariate and multivariate analyses indicated that poor performance status and the presence of extracranial metastases were poor prognostic factors related to overall survival. CONCLUSION: EGFR-TKI showed a favorable effect for EGFR-mutant NSCLC patients with CNS metastases. Prolonged TTF and CNS-PFS were observed with upfront brain radiotherapy.

    DOI: 10.1111/1759-7714.13189

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  • シラスタチンによりシスプラチン腎症を抑制することでシスプラチン投与を増量できる(Cilastatin suppresses cisplatin-induced nephrotoxicity and enables to increase the dose of cisplatin for cancer therapy)

    有田 将史, 渡部 聡, 青木 信将, 高橋 美帆, 庄子 聡, 野嵜 幸一郎, 市川 紘将, 近藤 利恵, 桑原 頌治, 田中 純太, 小屋 俊之, 斎藤 亮彦, 菊地 利明

    日本癌学会総会記事   78回   P - 1398   2019.9

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  • 小細胞肺癌患者におけるプロカルシトニンの臨床的意義に関する解析

    市川 紘将, 渡部 聡, 柳村 尚寛, 庄子 聡, 野嵜 幸一郎, 近藤 利恵, 青木 信将, 林 正周, 大嶋 康義, 小屋 俊之, 菊地 利明

    日本呼吸器学会誌   8 ( 増刊 )   336 - 336   2019.3

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  • Retrospective analysis of antitumor effects and biomarkers for nivolumab in NSCLC patients with EGFR mutations. International journal

    Miyuki Sato, Satoshi Watanabe, Hiroshi Tanaka, Koichiro Nozaki, Masashi Arita, Miho Takahashi, Satoshi Shoji, Kosuke Ichikawa, Rie Kondo, Nobumasa Aoki, Masachika Hayashi, Yasuyoshi Ohshima, Toshiyuki Koya, Riuko Ohashi, Yoichi Ajioka, Toshiaki Kikuchi

    PloS one   14 ( 4 )   e0215292   2019

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    Although the blockade of programmed cell death 1 (PD-1)/PD-ligand (L) 1 has demonstrated promising and durable clinical responses for non-small-cell lung cancers (NSCLCs), NSCLC patients with epidermal growth factor receptor (EGFR) mutations responded poorly to PD-1/PD-L1 inhibitors. Previous studies have identified several predictive biomarkers, including the expression of PD-L1 on tumor cells, for PD-1/PD-L1 blockade therapies in NSCLC patients; however, the usefulness of these biomarkers in NSCLCs with EGFR mutations has not been elucidated. The present study was conducted to evaluate the predictive biomarkers for PD-1/PD-L1 inhibitors in EGFR-mutated NSCLCs. We retrospectively analyzed 9 patients treated with nivolumab for EGFR-mutated NSCLCs. All but one patient received EGFR-tyrosine kinase inhibitors before nivolumab treatment. The overall response rate and median progression-free survival were 11% and 33 days (95% confidence interval (CI); 7 to 51), respectively. Univariate analysis revealed that patients with a good performance status (P = 0.11; hazard ratio (HR) 0.183, 95% CI 0.0217 to 1.549), a high density of CD4+ T cells (P = 0.136; HR 0.313, 95% CI 0.045 to 1.417) and a high density of Foxp3+ cells (P = 0.09; HR 0.264, 95% CI 0.0372 to 1.222) in the tumor microenvironment tended to have longer progression-free survival with nivolumab. Multivariate analysis revealed that a high density of CD4+ T cells (P = 0.005; HR<0.001, 95% CI <0.001 to 0.28) and a high density of Foxp3+ cells (P = 0.003; HR<0.001, 95% CI NA) in tumor tissues were strongly correlated with better progression-free survival. In contrast to previous studies in wild type EGFR NSCLCs, PD-L1 expression was not associated with the clinical benefit of anti-PD-1 treatment in EGFR-mutated NSCLCs. The current study indicated that immune status in the tumor microenvironment may be important for the effectiveness of nivolumab in NSCLC patients with EGFR mutations.

    DOI: 10.1371/journal.pone.0215292

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  • 小細胞肺癌患者におけるプロカルシトニンの臨床的意義に関する解析

    市川 紘将, 渡部 聡, 柳村 尚寛, 庄子 聡, 野嵜 幸一郎, 近藤 利恵, 青木 信将, 林 正周, 大嶋 康義, 小屋 俊之, 菊地 利明

    肺癌   58 ( 6 )   589 - 589   2018.10

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  • Transfer of in vitro-expanded naïve T cells after lymphodepletion enhances antitumor immunity through the induction of polyclonal antitumor effector T cells. International journal

    Tomohiro Tanaka, Satoshi Watanabe, Miho Takahashi, Ko Sato, Yu Saida, Junko Baba, Masashi Arita, Miyuki Sato, Aya Ohtsubo, Satoshi Shoji, Koichiro Nozaki, Kosuke Ichikawa, Rie Kondo, Nobumasa Aoki, Yasuyoshi Ohshima, Takuro Sakagami, Tetsuya Abe, Hiroshi Moro, Toshiyuki Koya, Junta Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, Toshiaki Kikuchi

    PloS one   12 ( 8 )   e0183976   2017

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    The adoptive transfer of effector T cells combined with lymphodepletion has demonstrated promising antitumor effects in mice and humans, although the availability of tumor-specific T cells is limited. We and others have also demonstrated that the transfer of polyclonal naïve T cells induces tumor-specific effector T cells and enhances antitumor immunity after lymphodepletion. Because tumors have been demonstrated to induce immunosuppressive networks and regulate the function of T cells, obtaining a sufficient number of fully functional naïve T cells that are able to differentiate into tumor-specific effector T cells remains difficult. To establish culture methods to obtain a large number of polyclonal T cells that are capable of differentiating into tumor-specific effector T cells, naïve T cells were activated with anti-CD3 mAbs in vitro. These cells were stimulated with IL-2 and IL-7 for the CD8 subset or with IL-7 and IL-23 for the CD4 subset. Transfer of these hyperexpanded T cells after lymphodepletion showed significant antitumor efficacy, and tumor-specific effector T cells were primed from these expanded T cells in tumor-bearing hosts. Moreover, these ex vivo-expanded T cells maintained T cell receptor diversity and showed long-term persistence of memory against specific tumors. Further analyses revealed that combination therapy consisting of vaccination with dendritic cells that were co-cultured with irradiated whole tumor cells and the transfer of ex vivo-expanded T cells significantly enhanced antitumor immunity. These results indicate that the transfer of ex vivo-expanded polyclonal T cells can be combined with other immunotherapies and augment antitumor effects.

    DOI: 10.1371/journal.pone.0183976

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  • Nephrotoxicity of cisplatin combination chemotherapy in thoracic malignancy patients with CKD risk factors. International journal

    Ko Sato, Satoshi Watanabe, Aya Ohtsubo, Satoshi Shoji, Daisuke Ishikawa, Tomohiro Tanaka, Koichiro Nozaki, Rie Kondo, Masaaki Okajima, Satoru Miura, Junta Tanaka, Takuro Sakagami, Toshiyuki Koya, Hiroshi Kagamu, Hirohisa Yoshizawa, Ichiei Narita

    BMC cancer   16   222 - 222   2016.3

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    BACKGROUND: Nephrotoxicity is the major side effect that limits the dose of cisplatin that can be safely administered, and it is a clinical problem in cancer patients who received cisplatin combination chemotherapy. Recent evidence has demonstrated that patients with chronic kidney disease (CKD) have an increased risk of developing acute kidney injury (AKI). The present study was conducted to evaluate the prevalence of CKD risk factors in patients who received cisplatin and to assess the correlation between CKD risk factors and cisplatin-induced AKI. METHODS: We retrospectively analyzed 84 patients treated with cisplatin combination chemotherapy for thoracic malignancies. AKI was defined as a decrease in the estimated glomerular filtration rate (eGFR) > 25% from base line, an increase in the serum creatinine (sCre) level of > 0.3 mg/dl or ≥ 1.5 times the baseline level. RESULTS: Eighty of the 84 patients (95.2%) had at least one risk factor for CKD. All enrolled patients received cisplatin with hydration, magnesium supplementation and mannitol. Cisplatin-induced AKI was observed in 18 patients (21.4%). Univariate analysis revealed that cardiac disease and use of non-steroidal anti-inflammatory drugs (NSAIDs) were associated with cisplatin-induced nephrotoxicity (odds ratios [OR] 6 and 3.56, 95% confidence intervals [CI] 1.21-29.87 and 1.11-11.39, p = 0.04 and p = 0.04, respectively). Multivariate analysis revealed that cisplatin nephrotoxicity occurred significantly more often in patients with both risk factors (OR 13.64, 95% CI 1.11-326.83, p = 0.04). Patients with more risk factors for CKD tended to have a greater risk of developing cisplatin-induced AKI. CONCLUSIONS: We should consider avoiding administration of cisplatin to patients with CKD risk factors, particularly cardiac disease and NSAID use.

    DOI: 10.1186/s12885-016-2271-8

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  • Critical Roles of Chemoresistant Effector and Regulatory T Cells in Antitumor Immunity after Lymphodepleting Chemotherapy. International journal

    Yu Saida, Satoshi Watanabe, Tomohiro Tanaka, Junko Baba, Ko Sato, Satoshi Shoji, Natsue Igarashi, Rie Kondo, Masaaki Okajima, Jun Koshio, Kosuke Ichikawa, Koichiro Nozaki, Daisuke Ishikawa, Toshiyuki Koya, Satoru Miura, Junta Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, Koh Nakata, Ichiei Narita

    Journal of immunology (Baltimore, Md. : 1950)   195 ( 2 )   726 - 35   2015.7

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    Antitumor immunity is augmented by cytotoxic lymphodepletion therapies. Adoptively transferred naive and effector T cells proliferate extensively and show enhanced antitumor effects in lymphopenic recipients. Although the impact of lymphodepletion on transferred donor T cells has been well evaluated, its influence on recipient T cells is largely unknown. The current study demonstrates that both regulatory T cells (Tregs) and effector CD8(+) T cells from lymphopenic recipients play critical roles in the development of antitumor immunity after lymphodepletion. Cyclophosphamide (CPA) treatment depleted lymphocytes more efficiently than other cytotoxic agents; however, the percentage of CD4(+)CD25(+) Foxp3(+) Tregs was significantly increased in CPA-treated lymphopenic mice. Depletion of these chemoresistant Tregs following CPA treatment and transfer of naive CD4(+) T cells augmented the antitumor immunity and significantly suppressed tumor progression. Further analyses revealed that recipient CD8(+) T cells were responsible for this augmentation. Using Rag2(-/-) mice or depletion of recipient CD8(+) T cells after CPA treatment abrogated the augmentation of antitumor effects in CPA-treated reconstituted mice. The transfer of donor CD4(+) T cells enhanced the proliferation of CD8(+) T cells and the priming of tumor-specific CD8(+) T cells originating from the lymphopenic recipients. These results highlight the importance of the recipient cells surviving cytotoxic regimens in cancer immunotherapies.

    DOI: 10.4049/jimmunol.1401468

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  • Advanced thymic cancer treated with carboplatin and paclitaxel in a patient undergoing hemodialysis.

    Satoru Miura, Hiroshi Kagamu, Takehito Sakai, Koichiro Nozaki, Katsuaki Asakawa, Hiroshi Moro, Masaaki Okajima, Satoshi Watanabe, Suguru Yamamoto, Noriaki Iino, Shin Goto, Junichiro James Kazama, Hirohisa Yoshizawa, Ichiei Narita

    Internal medicine (Tokyo, Japan)   54 ( 1 )   55 - 8   2015

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    A 53-year-old man with an asymptomatic anterior mediastinal tumor undergoing hemodialysis was referred to our institution. He was diagnosed with thymic basaloid carcinoma based on the findings of a chest tomography-guided biopsy and successfully treated with carboplatin (300 mg/m(2)/day) and paclitaxel (200 mg/m(2)/day) on day 1 for six three-week cycles. To our knowledge, this is the first report regarding the efficiency of a carboplatin dose-definition method based on the body surface area with paclitaxel in a hemodialysis patient. This report may therefore be useful for treating hemodialysis patients who are candidates for carboplatin and paclitaxel therapy.

    DOI: 10.2169/internalmedicine.54.3484

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  • DDX3X Induces Primary EGFR-TKI Resistance Based on Intratumor Heterogeneity in Lung Cancer Cells Harboring EGFR-Activating Mutations Reviewed

    Koichiro Nozaki, Hiroshi Kagamu, Satoshi Shoji, Natsue Igarashi, Aya Ohtsubo, Masaaki Okajima, Satoru Miura, Satoshi Watanabe, Hirohisa Yoshizawa, Ichiei Narita

    PLoS ONE   9 ( 10 )   e111019 - e111019   2014.10

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    DOI: 10.1371/journal.pone.0111019

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  • DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 3, X-linked is an immunogenic target of cancer stem cells. International journal

    Jun Koshio, Hiroshi Kagamu, Koichiro Nozaki, Yu Saida, Tomohiro Tanaka, Satoshi Shoji, Natsue Igarashi, Satoru Miura, Masaaki Okajima, Satoshi Watanabe, Hirohisa Yoshizawa, Ichiei Narita

    Cancer immunology, immunotherapy : CII   62 ( 10 )   1619 - 28   2013.10

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    Accumulating evidence suggests that most solid malignancies consist of heterogeneous tumor cells and that a relatively small subpopulation, which shares biological features with stem cells, survives through potentially lethal stresses such as chemotherapy and radiation treatment. Since the survival of this subpopulation of cancer stem cells (CSC) plays a critical role in recurrence, it must be eradicated in order to cure cancer. We previously reported that vaccination with CD133(+) murine melanoma cells exhibiting biological CSC features induced CSC-specific effector T cells. These were capable of eradicating CD133(+) tumor cells in vivo, thereby curing the parental tumor. In the current study, we indicated that DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 3, X-linked (DDX3X) is an immunogenic protein preferentially expressed in CD133(+) tumor cells. Vaccination with DDX3X primed specific T cells, resulting in protective and therapeutic antitumor immunity. The DDX3X-primed CD4(+) T cells produced CD133(+) tumor-specific IFNγ and IL-17 and mediated potent antitumor therapeutic efficacy. DDX3X is expressed in various human cancer cells, including lung, colon, and breast cancer cells. These results suggest that anti-DDX3X immunotherapy is a promising treatment option in efforts to eradicate CSC in the clinical setting.

    DOI: 10.1007/s00262-013-1467-x

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  • Depletion of radio-resistant regulatory T cells enhances antitumor immunity during recovery from lymphopenia. International journal

    Junko Baba, Satoshi Watanabe, Yu Saida, Tomohiro Tanaka, Takao Miyabayashi, Jun Koshio, Kosuke Ichikawa, Koichiro Nozaki, Toshiyuki Koya, Katsuya Deguchi, Chunrui Tan, Satoru Miura, Hiroshi Tanaka, Junta Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, Ko Nakata, Ichiei Narita

    Blood   120 ( 12 )   2417 - 27   2012.9

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    Cytotoxic lymphodepletion therapies augment antitumor immune responses. The generation and therapeutic efficacy of antitumor effector T cells (T(E)s) are enhanced during recovery from lymphopenia. Although the effects of lymphodepletion on naive T cells (T(N)s) and T(E)s have been studied extensively, the influence of lymphodepletion on suppressor cells remains poorly understood. In this study, we demonstrate a significant increase of CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) in sublethally irradiated lymphopenic mice. These radio-resistant Tregs inhibited the induction of T(E)s in tumor-draining lymph-nodes (TDLNs) during recovery from lymphopenia. The transfer of T(N)s into lymphopenic tumor-bearing mice resulted in some antitumor effects; however, Treg depletion after whole-body irradiation and reconstitution strongly inhibited tumor progression. Further analyses revealed that tumor-specific T cells were primed from the transferred T(N)s, whereas the Tregs originated from irradiated recipient cells. As in irradiated lymphopenic mice, a high percentage of Tregs was observed in cyclophosphamide-treated lymphopenic mice. The inhibition of Tregs in cyclophosphamide-treated mice significantly reduced tumor growth. These results indicate that the Tregs that survive cytotoxic therapies suppress antitumor immunity during recovery from lymphopenia and suggest that approaches to deplete radio and chemo-resistant Tregs can enhance cancer immunotherapies.

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Books

  • 肺癌薬物療法のエビデンスとコツ

    ( Role: Joint author ,  第6章 小細胞肺癌 「1.進展型のファーストライン」)

    株式会社 羊土社  2018.11 

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  • エビデンスに基づいた癌化学療法ハンドブック 2018

    大津 敦 総監修( Role: Joint author ,  非小細胞肺癌 「CBDCA+Nab-PTX」p142-144)

    株式会社 メディカルレビュー社  2018.6 

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  • 肺がん支持療法マニュアル

    山本信之 監修( Role: Joint author ,  4.神経障害 p60-62)

    株式会社 医薬ジャーナル  2017.10 

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MISC

  • Intra-tumor heterogeneityに基づくEGFR-TKI初期耐性機序の解明

    庄子 聡, 各務 博, 大坪 亜矢, 野嵜 幸一郎, 岡島 正明, 三浦 理, 渡部 聡, 小屋 俊之, 成田 一衛

    日本内科学会雑誌   104 ( Suppl. )   268 - 268   2015.2

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    DOI: 10.2169/naika.104.268

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  • Dendritic cell vaccination and regulatory T-cell depletion augment antitumor immunity after cytotoxic therapy

    Tomohiro Tanaka, Satoshi Watanabe, Ko Sato, Yu Saida, Junko Baba, Koichiro Nozaki, Daisuke Ishikawa, Natsue Igarashi, Satoshi Shoji, Masaaki Okajima, Satoru Miura, Junta Tanaka, Hiroshi Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, Ichiei Narita

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-2818

    Web of Science

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  • DDX3X induces signal switching to stem cell-specific Wnt/beta-catenin signaling, resulting in EGFR-TKI resistance in lung cancer cells harboring EGFR activating mutation

    Satoshi Shoji, Hiroshi Kagamu, Koichiro Nozaki, Natsue Igarashi, Masaaki Okajima, Satoru Miura, Satoshi Watanabe, Hrohisa Yoshizawa, Ichiei Narita

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-200

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  • DDX3X-specific effector T cells in small cell lung cancer patients reflect disease stage

    Natsue Igarashi, Hiroshi Kagamu, Koichiro Nozaki, Satoshi Shoji, Masaaki Okajima, Satoru Miura, Satoshi Watanabe, Hirohisa Yoshizawa, Ichiei Narita

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-2554

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  • 進展型小細胞肺癌に対するシスプラチン、ノギテカン、パクリタキセル、アムルビシン交替療法の第I相試験

    渡部 聡, 田中 純太, 佐藤 昂, 田中 知宏, 石川 大輔, 野嵜 幸一郎, 近藤 利恵, 岡島 正明, 三浦 理, 各務 博, 成田 一衛, 吉澤 弘久

    肺癌   54 ( 5 )   633 - 633   2014.10

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  • ゾレドロン酸、デノスマブを投与された非小細胞肺癌骨転移症例と、非骨転移症例の検討

    岡島 正明, 石川 大輔, 田中 知宏, 野嵜 幸一郎, 近藤 利恵, 三浦 理, 渡部 聡, 田中 純太, 吉澤 弘久, 各務 博, 成田 一衛

    肺癌   54 ( 5 )   541 - 541   2014.10

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  • 肺末梢病変に対するEBUS-GSを用いた気管支鏡検査の有用性の検討

    佐藤 昂, 渡部 聡, 岡島 正明, 石川 大輔, 田中 知宏, 野嵜 幸一郎, 近藤 利恵, 三浦 理, 田中 純太, 各務 博, 吉澤 弘久

    気管支学   36 ( 5 )   456 - 460   2014.9

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    背景. 近年、肺末梢の病変に対するガイドシース併用気管支腔内超音波断層法(EBUS-GS)の有用性と安全性が報告されている。また、肺癌治療の進歩に伴い組織型の確定や遺伝子検索の必要性が増し、組織採取が重要になってきている。目的. 今回我々は肺末梢病変に対するEBUS-GS併用気管支鏡検査の有用性を検討した。対象と方法. 2011年8月から2013年3月の20ヵ月間に、肺末梢病変に対してEBUS-GS併用下に気管支鏡検査を施行した64例を評価した。結果. 悪性腫瘍に対する正診率、感度はそれぞれ72.6%、66.7%であった。気管支鏡検査で肺腺癌と診断された症例でのEGFR遺伝子変異陽性率は33.3%であった。結論. EBUS-GS併用にて得られた検体は、肺癌組織型の確定診断や遺伝子検索に有用であると考えられた。(著者抄録)

    DOI: 10.18907/jjsre.36.5_456

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  • 癌多様性に基づいた新規EGFR-TKI耐性メカニズム(A novel EGFR-TKI resistance mechanism based on intratumor heterogeneity)

    庄子 聡, 各務 博, 野嵜 幸一郎, 岡島 正明, 三浦 理, 渡部 聡, 成田 一衛

    日本癌学会総会記事   73回   J - 1035   2014.9

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  • DDX3Xにより誘導される癌幹細胞様形質と新規EGFR-TKI耐性化メカニズム(DDX3X plays a critical role in a novel EGFR-TKI resistance mechanism correlating with CSC-like properties)

    庄子 聡, 各務 博, 野嵜 幸一郎, 五十嵐 夏恵, 才田 優, 田中 知宏, 近藤 利恵, 岡島 正明, 三浦 理, 渡部 聡, 吉澤 弘久, 成田 一衛

    日本癌学会総会記事   72回   332 - 332   2013.10

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  • シクロフォスファミドと化学療法耐性免疫抑制細胞の除去の組み合わせは優れた抗腫瘍効果を示す(Combination of cyclophosphamide and inhibition of chemo-resistant suppressor cells successfully treated advanced rumors)

    才田 優, 渡部 聡, 田中 知宏, 馬場 順子, 野嵜 幸一郎, 市川 紘将, 古塩 純, 三浦 理, 田中 純太, 各務 博, 吉沢 弘久, 成田 一衛

    日本癌学会総会記事   71回   282 - 282   2012.8

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  • DEAD/H(Asp-Glu-Ala-Asp/His)box polypeptide 3、X-linkedの癌幹細胞における役割(Oncogenic roles of DEAD/H (Asp-Glu-Ala-Asp/His) box polypeptide 3, X-linked)

    野嵜 幸一郎, 各務 博, 古塩 純, 市川 紘将, 才田 優, 田中 知宏, 渡部 聡, 吉沢 弘久, 成田 一衛

    日本癌学会総会記事   71回   135 - 135   2012.8

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  • Successful treatment of advanced tumors with chemo-immunotherapy: a combination of cyclophosphamide and inhibition of chemo-resistant immune suppressor cells

    Yu Saida, Satoshi Watanabe, Tomohiro Tanaka, Junko Baba, Koichiro Nozaki, Kosuke Ichikawa, Jun Koshio, Satoru Miura, Junta Tanaka, Hiroshi Kagamu, Hirohisa Yoshizawa, Ichiei Narita

    CANCER RESEARCH   72   2012.4

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    Language:English   Publishing type:Research paper, summary (international conference)   Publisher:AMER ASSOC CANCER RESEARCH  

    DOI: 10.1158/1538-7445.AM2012-1550

    Web of Science

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  • 癌幹細胞特異的蛋白質を用いた抗腫瘍免疫療法(DEAD/H box polypeptide 3, X-linked is a CD133+ tumor-specific protein and induces antitumor immunity)

    古塩 純, 各務 博, 成田 一衛, 中田 光, 吉澤 弘久, 田中 純太, 渡部 聡, 三浦 理, 宮林 貴大, 市川 紘将, 才田 優, 野嵜 幸一郎, 田中 知宏

    日本癌学会総会記事   70回   334 - 334   2011.9

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    Language:English   Publisher:日本癌学会  

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  • 癌免疫療法のコンディショニング 生体外で増やしたT細胞はリンパ球減少状態の宿主でエフェクター細胞に分化し抗腫瘍効果を示す(Conditioning for cancer immunotherapy: ex vivo expanded T cells effectively develop into effectors in lymphopenic hosts)

    才田 優, 渡部 聡, 馬場 順子, 田中 知宏, 野嵜 幸一郎, 市川 紘将, 古塩 純, 田中 純太, 各務 博, 吉澤 弘久, 成田 一衛

    日本癌学会総会記事   70回   260 - 260   2011.9

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  • Effectiveness of afatinib in an NSCLC patitent with EGFR mutation and primary resistance to osimertinib

    2021.2 

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    Event date: 2021.2

    Language:Japanese  

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