2024/02/22 更新

写真a

ニシジマ　ノブヒコ
西島　伸彦
nishijima nobuhiko
所属
武蔵小杉病院 呼吸器内科 助教
職名
助教
外部リンク

論文

  • 術後プラチナ併用化学療法後の再発非小細胞肺癌に対するプラチナ併用化学療法±ICIの有効性と安全性の検討

    久金 翔, 戸塚 猛大, 高橋 聡, 谷内 七三子, 西島 伸彦, 渥美 健一郎, 小齊平 聖治, 神尾 孝一郎, 岡野 哲也, 弦間 昭彦, 清家 正博, 廣瀬 敬

    肺癌   62 ( 6 )   593 - 593   2022年11月

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    記述言語：日本語   出版者・発行元：(NPO)日本肺癌学会  

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  • Resolution of bleomycin-induced murine pulmonary fibrosis via a splenic lymphocyte subpopulation. 査読 国際誌

    Koichiro Kamio, Arata Azuma, Kuniko Matsuda, Jiro Usuki, Minoru Inomata, Akemi Morinaga, Takeru Kashiwada, Nobuhiko Nishijima, Shioto Itakura, Nariaki Kokuho, Kenichiro Atsumi, Hiroki Hayashi, Tomoyoshi Yamaguchi, Kazue Fujita, Yoshinobu Saito, Shinji Abe, Kaoru Kubota, Akihiko Gemma

    Respiratory research   19 ( 1 )   71 - 71   2018年4月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive disease with high mortality, and the pathogenesis of the disease is still incompletely understood. Although lymphocytes, especially CD4+CD25+FoxP3+ regulatory T cells (Tregs), have been implicated in the development of IPF, contradictory results have been reported regarding the contribution of Tregs to fibrosis both in animals and humans. The aim of this study was to investigate whether a specific T cell subset has therapeutic potential in inhibiting bleomycin (BLM)-induced murine pulmonary fibrosis. METHODS: C57BL/6 mice received BLM (100 mg/kg body weight) with osmotic pumps (day 0), and pulmonary fibrosis was induced. Then, splenocytes or Tregs were adoptively transferred via the tail vein. The lungs were removed and subjected to histological and biochemical examinations to study the effects of these cells on pulmonary fibrosis, and blood samples were collected by cardiac punctures to measure relevant cytokines by enzyme-linked immunosorbent assay. Tregs isolated from an interleukin (IL)-10 knock-out mice were used to assess the effect of this mediator. To determine the roles of the spleen in this model, spleen vessels were carefully cauterized and the spleen was removed either on day 0 or 14 after BLM challenge. RESULTS: Splenocytes significantly ameliorated BLM-induced pulmonary fibrosis when they were administered on day 14. This effect was abrogated by depleting Tregs with an anti-CD25 monoclonal antibody. Adoptive transfer of Tregs on day 14 after a BLM challenge significantly attenuated pulmonary fibrosis, and this was accompanied by decreased production of fibroblast growth factor (FGF) 9-positive cells bearing the morphology of alveolar epithelial cells. In addition, BLM-induced plasma IL-10 expression reverted to basal levels after adoptive transfer of Tregs. Moreover, BLM-induced fibrocyte chemoattractant chemokine (CC motif) ligand-2 production was significantly ameliorated by Treg adoptive transfer in lung homogenates, accompanied by reduced accumulation of bone-marrow derived fibrocytes. Genetic ablation of IL-10 abrogated the ameliorating effect of Tregs on pulmonary fibrosis. Finally, splenectomy on day 0 after a BLM challenge significantly ameliorated lung fibrosis, whereas splenectomy on day 14 had no effect. CONCLUSIONS: These findings warrant further investigations to develop a cell-based therapy using Tregs for treating IPF.

    DOI： 10.1186/s12931-018-0783-2

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  • miR-200/ZEB axis regulates sensitivity to nintedanib in non-small cell lung cancer cells. 国際誌

    Nobuhiko Nishijima, Masahiro Seike, Chie Soeno, Mika Chiba, Akihiko Miyanaga, Rintaro Noro, Teppei Sugano, Masaru Matsumoto, Kaoru Kubota, Akihiko Gemma

    International journal of oncology   48 ( 3 )   937 - 44   2016年3月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Nintedanib (BIBF1120) is a multi-targeted angiokinase inhibitor and has been evaluated in idiopathic pulmonary fibrosis and advanced non-small cell lung cancer (NSCLC) patients in clinical studies. In the present study, we evaluated the antitumor effects of nintedanib in 16 NSCLC cell lines and tried to identify microRNA (miRNA) associated with sensitivity to nintedanib. No correlations between FGFR, PDGFR and VEGFR family activation and sensitivity to nintedanib were found. The difference in miRNA expression profiles between 5 nintedanib-sensitive and 5 nintedanib-resistant cell lines was evaluated by miRNA array and quantitative RT-PCR analysis (qRT-PCR). Expression of miR-200b, miR-200a and miR-141 belonging to the miR-200 family which contributes to epithelial-mesenchymal transition (EMT), was significantly lower in 5 nintedanib-resistant than in 5 nintedanib-sensitive cell lines. We examined the protein expression of EMT markers in these 10 NSCLC cell lines. E-cadherin expression was lower, and vimentin and ZEB1 expression were higher in 5 nintedanib-resistant cell lines. PC-1 was the most sensitive of the NSCLC cell lines to nintedanib. We established nintedanib-resistant PC-1 cells (PC-1R) by the stepwise method. PC-1R cells also showed decreased expression of miR-200b, miR-141 and miR-429 and increased expression of ZEB1 and ZEB2. We confirmed that induction of miR-200b or miR-141 enhanced sensitivity to nintedanib in nintedanib-resistant A549 and PC1-R cells. In addition, we evaluated the response to gefitinib in combination with nintedanib after TGF-β1 exposure of A549 cells. Nintedanib was able to reverse TGF-β1-induced EMT and resistance to gefitinib caused by miR-200b and miR-141 upregulation and ZEB1 downregulation. These results suggested that the miR-200/ZEB axis might be predictive biomarkers for sensitivity to nintedanib in NSCLC cells. Furthermore, nintedanib combined with gefitinib might be a novel therapeutic strategy for NSCLC cells with EMT phenotype and resistance to gefitinib.

    DOI： 10.3892/ijo.2016.3331

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  • Inhibition of ABCB1 Overcomes Cancer Stem Cell-like Properties and Acquired Resistance to MET Inhibitors in Non-Small Cell Lung Cancer. 査読 国際誌

    Sugano T, Seike M, Noro R, Soeno C, Chiba M, Zou F, Nakamichi S, Nishijima N, Matsumoto M, Miyanaga A, Kubota K, Gemma A

    Molecular cancer therapeutics   14 ( 11 )   2433 - 40   2015年11月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    DOI： 10.1158/1535-7163.MCT-15-0050

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  • Inhibition of ABCB1 overcomes cancer stem cell-like properties and acquired resistance to MET inhibitor in non-small cell lung cancer 査読

    Teppei Sugano, Masahiro Seike, Rintaro Noro, Chie Soeno, Shinji Nakamichi, Nobuhiko Nishijima, Masaru Matsumoto, Susumu Takeuchi, Akihiko Miyanaga, Kaoru Kubota, Akihiko Gemma

    CANCER RESEARCH   75   2015年8月

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    記述言語：英語   出版者・発行元：AMER ASSOC CANCER RESEARCH  

    DOI： 10.1158/1538-7445.AM2015-756

    Web of Science

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  • Distinct outcome of stage I lung adenocarcinoma with ACTN4 cell motility gene amplification 査読

    R. Noro, K. Honda, K. Tsuta, G. Ishii, A. M. Maeshima, N. Miura, K. Furuta, T. Shibata, H. Tsuda, A. Ochiai, T. Sakuma, N. Nishijima, A. Gemma, H. Asamura, K. Nagai, T. Yamada

    ANNALS OF ONCOLOGY   24 ( 10 )   2594 - 2600   2013年10月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：OXFORD UNIV PRESS  

    Even if detected at an early stage, a substantial number of lung cancers relapse after curative surgery. However, no method for distinguishing such tumors has yet been established.
    The copy number of the actinin-4 (ACTN4) gene was determined by fluorescence in situ hybridization on tissue microarrays comprising 543 surgically resected adenocarcinomas of the lung.
    Amplification (an increase in the copy number by >= 2.0 fold) of the ACTN4 gene was detected in two of seven lung adenocarcinoma cell lines and 79 (15%) of 543 cases of pathological stage I-IV lung adenocarcinoma. Multivariate analysis revealed that ACTN4 gene amplification was the most significant independent factor associated with an extremely high risk of death (hazard ratio, 6.78; P = 9.48 x 10(-5), Cox regression analysis) among 290 patients with stage I lung adenocarcinoma. The prognostic significance of ACTN gene amplification was further validated in three independent cohorts totaling 1033 patients.
    Amplification of the ACTN4 gene defines a small but substantial subset of patients with stage I lung adenocarcinoma showing a distinct outcome. Such patients require intensive medical attention and might benefit from postoperative adjuvant chemotherapy.

    DOI： 10.1093/annonc/mdt293

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  • Cancer-initiating cell marker-positive cells generate metastatic tumors that recapitulate the histology of the primary tumors. 国際誌

    Nobuhiko Nishijima, Genichiro Ishii, Kanji Nagai, Naho Atsumi, Keiju Aokage, Yuichi Tokunaga, Hideomi Ichinokawa, Yuichiro Ohe, Atsushi Ochiai

    Pathology international   63 ( 2 )   94 - 101   2013年2月

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    記述言語：英語   掲載種別：研究論文（学術雑誌）  

    Cancer-initiating cell (CIC) hypothesis suggests that CICs may be responsible for the generation of tumors that recapitulate the histology of the primary tumor at distant sites. We investigated the distribution of CIC markers (podoplanin (PDPN), CD44, and p63) positive cells of lung squamous cell carcinoma (SqCC) within primary and matched lymph node (LN) metastatic tumors to confirm this hypothesis (n = 113). In 61 cases, the PDPN-positive cells were localized in more peripheral areas of the tumor nests than the CD44- and p63-positive cells. This distribution pattern corresponded to a 'hierarchical distribution (HD)' reported previously. Among the cases with HD-(+) primary tumors (n = 61), the number showing HD-(+) LN metastatic tumors was 31 (51%), while among the cases with HD-(-) primary tumors (n = 52), the number showing HD-(+) LN metastatic tumors was 7 (13%) (p < 0.01). Primary and matched pulmonary metastatic (PM) tumors were also analyzed (n = 31), and a significant relationship of the HD pattern between them was also detected (p = 0.01). These results indicate that PDPN-positive cells might reflect the most immature cells in the differentiation process of metastatic SqCC and might generate metastatic tumors that recapitulate the histologic heterogeneity of the primary tumor.

    DOI： 10.1111/pin.12039

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  • High copy number of the MET gene predicts resistance to EGFR-TKI in non-small cell lung cancer patients. 査読

    Rintaro Noro, Masahiro Seike, Chie Soeno, Kuniko Matsuda, Teppei Sugano, Nobuhiko Nishijima, Masaru Toyokawa, Kazuhiro Kitamura, Seiji Kosaihira, Yuji Minegishi, Akinobu Yoshimura, Kaoru Kubota, Akihiko Gemma

    CANCER RESEARCH   72   2012年4月

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    記述言語：英語   出版者・発行元：AMER ASSOC CANCER RESEARCH  

    DOI： 10.1158/1538-7445.AM2012-5548

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