Updated on 2025/02/12

写真a

 
nishijima nobuhiko
 
Affiliation
Musashikosugi Hospital, Department of Pulmonary Medicine, Assistant Professor
Title
Assistant Professor
External link

Research Interests

  • lung cancer

Papers

  • Streptococcal Toxic Shock Syndrome with Multiple Cerebral Infarctions Caused by Streptococcus dysgalactiae subsp. equisimilis: An Autopsy Case Report. Reviewed

    Sho Saito, Namiko Taniuchi, Norio Motoda, Kanta Tsunoda, Junpei Sato, Takahiro Suzuki, Junichi Aoyama, Nobuhiko Nishijima, Masahiro Seike, Yoshinobu Saito

    Internal medicine (Tokyo, Japan)   2024.7

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    We herein report an autopsy case of streptococcal toxic shock syndrome with disseminated intravascular coagulation and multiple cerebral infarctions induced by Streptococcus dysgalactiae subsp. equisimilis (STSS) in an 84-year-old male. Pathological examination revealed sepsis with hemophagocytosis in the reticular system and intravascular bacteria in multiple organs, originating from bacterial necrotizing fasciitis of the lower extremities. The brain MRI findings showed a DWI-FLAIR mismatch, whereas the pathology was almost normal, thus supporting a hyperacute phase of cerebral infarction. The findings in this case help to elucidate the pathogenesis of STSS and develop appropriate treatment strategies.

    DOI: 10.2169/internalmedicine.3640-24

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  • Interstitial lung disease with prolonged fever that occurred during long-term administration of olaparib in a 74-year-old ovarian cancer patient: Radiological features and considerations for preventing delayed diagnosis. International journal

    Yoshinobu Saito, Rei Yamaguchi, Takahiro Suzuki, Junpei Sato, Nobuhiko Nishijima, Sho Saito, Junichi Aoyama, Namiko Taniuchi, Masahiro Seike, Noriyuki Katsumata

    Radiology case reports   19 ( 6 )   2100 - 2105   2024.6

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    A 74-year-old woman, who had been receiving olaparib for the treatment of ovarian cancer for more than a year, visited the emergency department complaining of a fever that had lasted for 1 month. She had been taking antipyretics and antibiotics for her fever, but without any effect. Although she had no symptoms other than fever, she had stopped taking olaparib for 1 week before her visit because she had developed anemia caused by myelosuppression from olaparib. After discontinuing olaparib, her maximum body temperature decreased. On admission, chest X-ray revealed no abnormalities, but chest CT showed diffuse ground-glass opacities. Chest CT taken 5 days later showed partial improvement; therefore, we diagnosed her with interstitial lung disease (ILD) associated with olaparib. After short-term steroid treatment, the ground-glass opacities disappeared, and the patient became afebrile. The CT scan taken for tumor evaluation 2 days before the onset of fever showed a few centrilobular nodular opacities and small patchy ground-glass opacities. These findings could indicate early lesions of ILD, but they seemed inconspicuous and nonspecific, and it might have been difficult to diagnose ILD then. To date, few cases of ILD associated with olaparib have been reported. However, based on previous reports, fever is often seen, and CT findings mainly comprise diffuse ground-glass opacities, and in some cases, centrilobular nodular shadows. Thus, in conjunction with the findings of the present case, these characteristics may be representative of olaparib-induced ILD.

    DOI: 10.1016/j.radcr.2024.02.064

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  • 特発性肺線維症/進行性肺線維症に対する抗線維化薬の導入遅延・治療継続阻害に関わる因子についての検討

    齊藤 翔, 青山 純一, 谷内 七三子, 鈴木 貴大, 佐藤 純平, 西島 伸彦, 清家 正博, 齋藤 好信

    日本呼吸器学会誌   13 ( 増刊 )   315 - 315   2024.3

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  • A Case of Immune Aplastic Anemia during Combined Treatment with Atezolizumab and Chemotherapy for Non-Small Cell Lung Cancer.

    Satoru Matsuki, Namiko Taniuchi, Naoko Okada, Junpei Sato, Nobuhiko Nishijima, Koichiro Kamio, Norio Motoda, Muneo Okamoto, Masahiro Seike, Arata Azuma

    Journal of Nippon Medical School = Nippon Ika Daigaku zasshi   91 ( 3 )   339 - 346   2024

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    Immune check point inhibitors (ICIs) have durable antitumor effects. However, autoimmune toxicities, termed immune-related adverse events, occur in some patients. We report a case of severe immune aplastic anemia (AA) in a patient with non-small cell lung cancer who was receiving atezolizumab with bevacizumab/carboplatin/paclitaxel. Although the cancer has not recurred, his bone marrow is depleted and he did not respond to immunosuppressive therapy. He has survived for 1.5 years with blood transfusions and infection control. Immune AA associated with ICIs is rare, and a treatment has not yet been established. This case report provides information on the management and treatment response of patients with AA caused by ICIs. Further studies should investigate the mechanism and pathogenesis of immune AA caused by ICIs.

    DOI: 10.1272/jnms.JNMS.2024_91-302

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  • Platinum-combination chemotherapy with or without immune-checkpoint inhibitor in patients with postoperative recurrent non-small cell lung cancer previously treated with adjuvant platinum-doublet chemotherapy: A multicenter retrospective study. International journal

    Kakeru Hisakane, Takehiro Tozuka, Satoshi Takahashi, Namiko Taniuchi, Nobuhiko Nishijima, Kenichiro Atsumi, Tetsuya Okano, Masahiro Seike, Takashi Hirose

    Thoracic cancer   14 ( 21 )   2069 - 2076   2023.7

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    BACKGROUND: Rechallenge with platinum-combination chemotherapy in patients with advanced non-small cell lung cancer (NSCLC) after disease progression on platinum-combination chemotherapy occasionally leads to a favorable response. The efficacy and safety of platinum-combination chemotherapy with or without immune-checkpoint inhibitor (ICI) for patients with recurrent NSCLC after surgery followed by adjuvant platinum-doublet chemotherapy remains uncertain. METHODS: Patients who relapsed after surgery plus adjuvant platinum-doublet chemotherapy and received platinum-combination chemotherapy with or without ICI between April 2011 and March 2021 at four Nippon Medical School hospitals were retrospectively analyzed. RESULTS: Among 177 patients who received adjuvant platinum-doublet chemotherapy after surgery, a total of 30 patients who received platinum-combination rechemotherapy with or without ICI after relapse were included in this study. Seven patients received ICI-combined chemotherapy. The median disease-free survival (DFS) after surgery was 13.6 months. The objective response rate and disease-control rate were 46.7% and 80.0%, respectively. The median progression-free survival and overall survival were 10.2 and 37.5 months, respectively. Patients with longer DFS (≥12 months) had a better prognosis than others. The most common grade ≥3 toxicity associated with this treatment was neutropenia (33%). Grade ≥3 immune-related adverse events were pneumonitis (14%) and colitis (14%). Treatment-related deaths did not occur in this study. CONCLUSION: Platinum-combination chemotherapy with or without ICI for patients with postoperative recurrent NSCLC who previously received adjuvant platinum-doublet chemotherapy was effective and safe. In particular, this therapy may be promising for patients with longer DFS.

    DOI: 10.1111/1759-7714.14992

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  • 特発性肺線維症に対する早期治療介入への障壁に関する研究

    佐藤 純平, 神尾 孝一郎, 谷内 七三子, 櫻井 侑美, 西島 伸彦, 齋藤 好信, 清家 正博, 吾妻 安良太

    日本呼吸器学会誌   12 ( 増刊 )   218 - 218   2023.3

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  • Pulmonary sarcoidosis complicated by rheumatoid arthritis in a patient presenting with progressive fibrosing interstitial lung disease and treated with nintedanib: a case report and literature review. International journal

    Ayana Suzuki, Koichiro Kamio, Mitsuhiro Takeno, Yasuhiro Terasaki, Namiko Taniuchi, Junpei Sato, Nobuhiko Nishijima, Yoshinobu Saito, Masahiro Seike, Akihiko Gemma, Arata Azuma

    Therapeutic advances in respiratory disease   17   17534666231158279 - 17534666231158279   2023

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    Sarcoidosis is a multisystem disease with an unknown etiology and is characterized by the formation of noncaseating granulomas in the affected organs. We present the case of a 69-year-old male Japanese patient with bilateral hilar lymphadenopathy on chest radiographs for more than 10 years, left without further investigation. The patient reported no clinical symptoms. Chest computed tomography revealed ground-glass opacities and reticular shadows in both lungs, along with bilateral hilar and mediastinal lymphadenopathy. Lymphocytosis was observed in bronchoalveolar lavage fluid. Pathological examination of transbronchial lung biopsy revealed noncaseating, epithelioid granulomas congruous with sarcoidosis, together with other findings. There were no abnormalities on electrocardiogram, echocardiogram, and ophthalmic examination.For progressive dyspnea on exertion, systemic corticosteroid therapy with oral prednisolone (25 mg/day) was initiated in 2017 and gradually tapered. Despite this intervention, the decline in forced vital capacity (FVC) was accelerated. Three years later, the patient noticed swelling in his right wrist. Further investigation revealed elevated anti-cyclic citrullinated peptide antibodies and absence of noncaseating epithelioid granuloma on surgical biopsy, leading to the diagnosis of rheumatoid arthritis (RA). Thereafter, the anti-fibrotic agent nintedanib was initiated, because interstitial lung disease (ILD) was considered to have converted into a progressive fibrosing phenotype (PF-ILD) with overlapping RA-associated lung involvement. With treatment, the progression of decline in FVC was slowed, although home oxygen therapy was introduced.

    DOI: 10.1177/17534666231158279

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  • 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   2022.11

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  • サルコイドーシスの経過中に関節リウマチを発症し、進行するILDに対しニンテダニブの投与を必要とした症例

    鈴木 彩奈, 神尾 孝一郎, 岳野 光弘, 寺崎 泰弘, 谷内 七三子, 西島 伸彦, 佐藤 純平, 齋藤 好信, 清家 正博, 吾妻 安良太

    日本サルコイドーシス/肉芽腫性疾患学会雑誌   42 ( サプリメント号 )   65 - 65   2022.10

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  • 次々に薬剤耐性を獲得した緑膿菌による重症肺炎の1例

    加藤 滉介, 谷内 七三子, 三澤 一仁, 鈴木 貴大, 櫻井 侑美, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 吾妻 安良太, 清家 正博

    日本内科学会関東地方会   680回   47 - 47   2022.9

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  • 非挿管管理中に著明な縦隔気腫をきたしたCOVID-19肺炎の一例

    中原 匡一, 谷内 七三子, 吉野 雄大, 三上 恵莉花, 宮寺 恵希, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 清家 正博, 弦間 昭彦, 吾妻 安良太

    日本結核・非結核性抗酸菌症学会関東支部学会・日本呼吸器学会関東地方会合同学会プログラム・抄録集   181回・248回   15 - 15   2022.2

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  • COVID-19肺炎との鑑別を要した抗MDA5抗体陽性間質性肺炎の1例

    梁井 由香子, 谷内 七三子, 三宅 絵里佳, 鈴木 彩奈, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 清家 正博, 弦間 昭彦, 吾妻 安良太

    日本内科学会関東地方会   671回   58 - 58   2021.9

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  • 自家骨髄細胞による肺線維症モデルマウスの病態改善効果に関する研究

    神尾 孝一郎, 吾妻 安良太, 松田 久仁子, 猪俣 稔, 久世 眞之, 臼杵 二郎, 田中 徹, 柏田 建, 佐藤 純平, 西島 伸彦, 渥美 健一郎, 齋藤 好信, 清家 正博, 弦間 昭彦

    日本呼吸器学会誌   10 ( 増刊 )   179 - 179   2021.4

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  • COVID-19肺炎との鑑別を要した非HIVニューモシスチス肺炎の1例

    鈴木 彩奈, 谷内 七三子, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 吾妻 安良太, 清家 正博, 弦間 昭彦

    日本内科学会関東地方会   666回   47 - 47   2021.2

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  • Whole-exome and RNA sequencing of pulmonary carcinoid reveals chromosomal rearrangements associated with recurrence. Reviewed International journal

    Akihiko Miyanaga, Mari Masuda, Noriko Motoi, Koji Tsuta, Yuka Nakamura, Nobuhiko Nishijima, Shun-Ichi Watanabe, Hisao Asamura, Akihiko Tsuchida, Masahiro Seike, Akihiko Gemma, Tesshi Yamada

    Lung cancer (Amsterdam, Netherlands)   145   85 - 94   2020.7

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    INTRODUCTION: The majority of pulmonary carcinoid (PC) tumors can be cured by surgical resection alone, but a significant proportion of patients experience recurrence. As PC is insensitive to conventional chemotherapy, further clarification of the molecular mechanisms of metastasis is needed in order to develop targeted therapeutics. METHODS: We performed comprehensive whole-exome sequencing (WES) of primary tumors and corresponding normal lung tissues from 14 PC patients (including 4 patients who developed postsurgical distant metastasis) and RNA sequencing of primary tumors from 6 PC patients (including 4 patients who developed postsurgical distant metastasis). Exon array-based gene expression analysis was performed in 25 cases of PC. RESULTS: We identified a total of 139 alterations in 136 genes. MUC6 and SPTA1 were recurrently mutated at a frequency of 21% (3/14) and 14% (2/14), respectively. Mucin protein family genes including MUC2, MUC4 and MUC6 were mutated in a mutually exclusive manner in 36% (5/14). Pathway analysis of the mutated genes revealed enrichment of genes involved in mitogen-activated protein kinase (MAPK) signaling, regulation of the actin cytoskeleton and focal adhesion, and transforming growth factor (TGF)-β signaling. RNA sequencing revealed a total of 8 novel fusion transcripts including one derived from a chromosomal translocation between the TRIB2 and PRKCE genes. All of the 8 fusion genes were detected in primary PCs that had developed metastasis after surgical resection. We identified 14 genes (DENND1B, GRID1, CLMN, DENND1B, NRP1, SEL1L3, C5orf13, TNFRSF21, TES, STK39, MTHFD2, OPN3, MET, and HIST1H3C) up-regulated in 5 PCs that had relapsed after surgical resection. CONCLUSIONS: In this study we identified novel somatic mutations and chromosomal rearrangements in PC by examining clinically aggressive cases that had developed postsurgical metastasis. It will be essential to validate the clinical significance of these genetic changes in a larger independent patient cohort.

    DOI: 10.1016/j.lungcan.2020.03.027

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  • Resolution of bleomycin-induced murine pulmonary fibrosis via a splenic lymphocyte subpopulation. Reviewed International journal

    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   2018.4

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    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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  • XPLN is modulated by HDAC inhibitors and negatively regulates SPARC expression by targeting mTORC2 in human lung fibroblasts Reviewed

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

    PULMONARY PHARMACOLOGY & THERAPEUTICS   44   61 - 69   2017.6

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    Pathogenesis of idiopathic pulmonary fibrosis (IPF) remains unclear. Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein that participates in the assembly and turnover of the extra cellular matrix, whose expression is regulated by transforming growth factor (TGF)-beta 1 through activation of mammalian target of rapamycin complex 2 (mTORC2). Exchange factor found in platelets, leukemic, and neuronal tissues (XPLN) is an endogenous inhibitor of mTORC2. However, whether XPLN modulates SPARC expression remains unknown. Herein, we investigated the regulatory mechanisms of XPLN in human lung fibroblasts. Effect of XPLN on mTORC2 activity was evaluated by silencing XPLN in human foetal lung fibroblasts (HFL-1 cells), using small interfering RNA. SPARC expression was quantified by quantitative real-time RT-PCR and western blotting. Fibroblasts were treated with TGF-beta 1, histone deacetylase (HDAC) inhibitors, entinostat, or vorinostat, to assess their effects on XPLN expression. Moreover, the effect of mTORC1 inhibition on SPARC and XPLN was examined. XPLN depletion stimulated SPARC expression and Akt phosphorylation on Ser473. TGF-beta 1 treatment down-regulated XPLN via Smad 2/3. XPLN mRNA expression was up-regulated upon treatment with HDAC inhibitors in a concentration dependent manner, and TGF-beta 1-induced SPARC expression was reversed by entinostat treatment. mTORC1 inhibition by rapamycin and Raptor depletion stimulated SPARC expression. In conclusion, this is the first study describing the involvement of XPLN in the regulation of SPARC. These findings may help uncover the regulatory mechanisms of the mTORC2-SPARC axis. The up-regulation of XPLN by HDAC inhibitors may be a novel therapeutic approach in patients with IPF. (C) 2017 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.pupt.2017.03.003

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

    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   2016.3

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    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. Reviewed International journal

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

    Molecular cancer therapeutics   14 ( 11 )   2433 - 40   2015.11

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    Patients with non-small cell lung cancer (NSCLC) EGFR mutations have shown a dramatic response to EGFR inhibitors (EGFR-TKI). EGFR T790M mutation and MET amplification have been recognized as major mechanisms of acquired resistance to EGFR-TKI. Therefore, MET inhibitors have recently been used in NSCLC patients in clinical trials. In this study, we tried to identify the mechanism of acquired resistance to MET inhibitors. We analyzed the antitumor effects of two MET inhibitors, PHA-665752 and crizotinib, in 10 NSCLC cell lines. EBC-1 cells with MET amplification were the only cells that were sensitive to both MET inhibitors. We established PHA-665752-resistant EBC-1 cells, namely EBC-1R cells. Activation of KRAS, EGFR, and FGFR2 signaling was observed in EBC-1R cells by FISH and receptor tyrosine kinase phosphorylation antibody arrays. EBC-1R cells also showed overexpression of ATP-binding cassette subfamily B member 1 (ABCB1) as well as phosphorylation of MET. EBC-1R cells grew as cell spheres that exhibited cancer stem cell-like (CSC) properties and epithelial-mesenchymal transition (EMT). The level of miR-138 that targeted ABCB1 was decreased in EBC-1R cells. ABCB1 siRNA and the ABCB1 inhibitor elacridar could reduce sphere numbers and suppress EMT. Elacridar could also reverse resistance to PHA-665752 in EBC-1R cells. Our study demonstrated that ABCB1 overexpression, which was associated with CSC properties and EMT, was involved in the acquired resistance to MET inhibitors. Inhibition of ABCB1 might be a novel therapeutic strategy for NSCLC patients with acquired resistance to MET inhibitors.

    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 Reviewed

    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   2015.8

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    DOI: 10.1158/1538-7445.AM2015-756

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  • MET FISH-positive status predicts short progression-free survival and overall survival after gefitinib treatment in lung adenocarcinoma with EGFR mutation. Reviewed International journal

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

    BMC cancer   15   31 - 31   2015.2

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    BACKGROUND: Lung adenocarcinoma patients with EGFR gene mutations have shown a dramatic response to gefitinib. However, drug resistance eventually emerges which limits the mean duration of response. With that in view, we examined the correlations between MET gene status as assessed by fluorescence in situ hybridization (FISH) with overall survival (OS) and progression-free survival (PFS) in adenocarcinoma patients with EGFR gene mutations who had received gefitinib therapy. METHODS: We evaluated 35 lung cancer samples with EGFR mutation from adenocarcinoma patients who had received gefitinib. Gene copy numbers (GCNs) and amplification of MET gene before gefitinib therapy was examined by FISH. MET protein expression was also evaluated by immunohistochemistry (IHC). RESULTS: FISH assessment showed that of the 35 adenocarcinoma samples, 10 patients (29%) exhibited high polysomy (5 copies≦mean MET per cell) and 1 patient (3%) exhibited amplification (2≦MET gene (red)/CEP7q (green) per cell). IHC evaluation of MET protein expression could not confirm MET high polysomy status. The Eleven patients with MET FISH positivity had significantly shorter progression-free survival (PFS) and overall survival (OS) than the 24 patients who were MET FISH-negative (PFS: p = 0.001 and OS: p = 0.03). Median PFS and OS with MET FISH-positivity were 7.6 months and 16.8 months, respectively, whereas PFS and OS with MET FISH-negativity were 15.9 months and 33.0 months, respectively. Univariate analysis revealed that MET FISH-positivity was the most significant independent factor associated with a high risk of progression and death (hazard ratio, 3.83 (p = 0.0008) and 2.25 (p = 0.03), respectively). CONCLUSIONS: Using FISH analysis to detect high polysomy and amplification of MET gene may be useful in predicting shortened PFS and OS after Gefitinib treatment in lung adenocarcinoma. The correlation between MET gene status and clinical outcomes for EGFR-TKI should be further evaluated using large scale samples.

    DOI: 10.1186/s12885-015-1019-1

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  • Significance of osteopontin in the sensitivity of malignant pleural mesothelioma to pemetrexed. Reviewed International journal

    Susumu Takeuchi, Masahiro Seike, Rintaro Noro, Chie Soeno, Teppei Sugano, Fenfei Zou, Haruka Uesaka, Nobuhiko Nishijima, Masaru Matsumoto, Yuji Minegishi, Kaoru Kubota, Akihiko Gemma

    International journal of oncology   44 ( 6 )   1886 - 94   2014.6

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    Pemetrexed (PEM) is currently recommended as one of the standard anticancer drugs for malignant pleural mesothelioma (MPM). However, the mechanism of the sensitivity of MPM to PEM remains unclear. We analyzed the antitumor effects of PEM in six MPM cell lines by MTS assay. To identify genes associated with drug sensitivity, we conducted gene expression profiling on the same set of cell lines using GeneChips and pathway analysis. Three cell lines were sensitive to PEM. A total fo 18 transcripts and 14 genes identified by GeneChips were significantly correlated with sensitivity to PEM. Pathway analysis revealed that osteopontin (SPP1/OPN) was an important target in PEM sensitivity. Overexpression of SPP1/OPN was observed in the sensitive cells by quantitative PCR and western blot analysis. Introduction of SPP1/OPN by lentiviral vector significantly enhanced the invasion activities of MPM cells. PEM treatment with SPP1/OPN knockdown inhibited the PEM-induced cell growth-inhibitory effect in PEM-sensitive cells. Expression of SPP1/OPN and AKT phosphorylation significantly decreased after PEM treatment of the PEM-sensitive cells. High immunohistochemical expression of SPP1/OPN was observed in two of three MPM patients who had a partial response to PEM-based chemotherapy. PEM has antitumor effects in MPM cells dependent on SPP1/OPN overexpression resulting in AKT activation. Our results suggest that SPP1 may be used as a single predictive biomarker of the effectiveness of PEM treatment in MPM.

    DOI: 10.3892/ijo.2014.2370

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

    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   2013.10

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    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. International journal

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

    Pathology international   63 ( 2 )   94 - 101   2013.2

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    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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  • Bevacizumab plus chemotherapy for advanced non-squamous non-small-cell lung cancer with malignant pleural effusion. Reviewed International journal

    Kazuhiro Kitamura, Kaoru Kubota, Masahiro Ando, Satoshi Takahashi, Nobuhiko Nishijima, Teppei Sugano, Masaru Toyokawa, Koji Miwa, Seiji Kosaihira, Rintaro Noro, Yuji Minegishi, Masahiro Seike, Akinobu Yoshimura, Akihiko Gemma

    Cancer chemotherapy and pharmacology   71 ( 2 )   457 - 61   2013.2

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    PURPOSE: The presence of malignant pleural effusion (MPE) indicates a poorer prognosis for patients with non-small-cell lung cancer (NSCLC) and impairs their quality of life. Because vascular endothelial growth factor (VEGF) is the key mediator MPE production, we evaluated the efficacy and safety of chemotherapy plus bevacizumab, an anti-VEGF antibody, in non-squamous NSCLC patients with MPE, especially regarding the control of pleural effusions. METHODS: From November 1, 2009 to September 30, 2011, medical charts of 13 consecutive patients with MPE who received bevacizumab plus chemotherapy as the initial or secondary treatment were retrospectively analyzed. RESULTS: Of the 13 patients, 6 did not undergo pleurodesis, 3 were unsuccessfully treated by pleurodesis, 2 had encapsulated pleural effusion, and 2 had no re-expansion of the lung. Twelve patients (92.3 %) achieved MPE control lasting >8 weeks following bevacizumab plus chemotherapy. Five of 10 patients with measurable lesions had confirmed partial responses. Of 3 patients without measurable lesions, one had confirmed CR. Median progression-free survival time without re-accumulation of MPE was 312 days. Grade 3 or 4 neutropenia, thrombocytopenia, hypertension, or proteinuria was observed in 2, 2, 1, or 1 patient, respectively. CONCLUSIONS: This is the first study to report that bevacizumab plus chemotherapy is highly effective for the management of MPE in non-squamous NSCLC patients. Prospective clinical trials are warranted to investigate the efficacy of bevacizumab for MPE.

    DOI: 10.1007/s00280-012-2026-4

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  • MECHANISMS OF ACQUIRED RESISTANCE TO MTOR INHIBITOR IN SMALL CELL LUNG CANCER Reviewed

    Toyokawa Masaru, Noro Rintaro, Seike Masahiro, Nishijima Nobuhiko, Kitamura Kazuhiro, Minegishi Yuji, Soeno Chie, Matsuda Kuniko, Kubota Kaoru, Gemma Akihiko

    JOURNAL OF THORACIC ONCOLOGY   7 ( 11 )   S465 - S465   2012.11

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  • MET FISH POSITIVE PREDICTS THE RESISTANCE TO EGFR-TKI IN NON-SMALL LUNG CANCER PATIENTS. Reviewed

    Noro Rintaro, Seike Masahiro, Soeno Chie, Matsuda Kuniko, Sugano Teppei, Kitamura Kazuhiro, Nishijima Nobuhiko, Kosaihira Seni, Minegishi Yuji, Kubota Kaoru, Gemma Akihiko

    JOURNAL OF THORACIC ONCOLOGY   7 ( 11 )   S468   2012.11

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

    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   2012.4

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    DOI: 10.1158/1538-7445.AM2012-5548

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  • AMPLIFICATION OF THE ACTN4 GENE IN STAGE I ADENOCARCINOMA OF THE LUNG Reviewed

    Rintaro Noro, Kazufumi Honda, Koji Tsuta, Genichiro Ishii, Akiko M. Maeshima, Koh Furuta, Tatsuhiro Shibata, Hitoshi Tsuda, Atsushi Ochiai, Tomohide Sakuma, Nobuhiko Nishijima, Akihiko Gemma, Hisao Asamura, Kanji Nagai, Tesshi Yamada

    JOURNAL OF THORACIC ONCOLOGY   6 ( 6 )   S959 - S959   2011.6

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Misc.

  • Barriers in early intervention and failed continuation for IPF/PPF

    齊藤翔, 青山純一, 谷内七三子, 鈴木貴大, 佐藤純平, 西島伸彦, 清家正博, 齋藤好信

    日本呼吸器学会誌(Web)   13   2024

  • F.necrophorumによる膿胸及び敗血症を呈しLemierre症候群が疑われた若年男性の一例

    前川 良, 谷内 七三子, 齊藤 翔, 青山 純一, 山口 玲, 佐藤 純平, 西島 伸彦, 清家 正博, 齋藤 好信

    日本結核・非結核性抗酸菌症学会関東支部学会・日本呼吸器学会関東地方会合同学会プログラム・抄録集   184回・256回   24 - 24   2023.9

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  • 特発性肺線維症に対する早期治療介入への障壁に関する研究

    佐藤 純平, 神尾 孝一郎, 谷内 七三子, 櫻井 侑美, 西島 伸彦, 齋藤 好信, 清家 正博, 吾妻 安良太

    日本呼吸器学会誌   12 ( 増刊 )   218 - 218   2023.3

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  • 多彩な合併症を呈し治療に難渋した重症喘息の一例

    朽名 紗智子, 谷内 七三子, 三澤 一仁, 磯 博和, 櫻井 侑美, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 清家 正博, 吾妻 安良太

    日本結核・非結核性抗酸菌症学会関東支部学会・日本呼吸器学会関東地方会合同学会プログラム・抄録集   183回・253回   17 - 17   2023.2

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  • 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   2022.11

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  • 次々に薬剤耐性を獲得した緑膿菌による重症肺炎の1例

    加藤 滉介, 谷内 七三子, 三澤 一仁, 鈴木 貴大, 櫻井 侑美, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 吾妻 安良太, 清家 正博

    第680回日本内科学会関東地方会   680回   47 - 47   2022.9

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  • 非挿管管理中に著明な縦隔気腫をきたしたCOVID-19肺炎の一例

    中原 匡一, 谷内 七三子, 吉野 雄大, 三上 恵莉花, 宮寺 恵希, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 清家 正博, 弦間 昭彦, 吾妻 安良太

    日本結核・非結核性抗酸菌症学会関東支部学会・日本呼吸器学会関東地方会合同学会プログラム・抄録集   181回・248回   15 - 15   2022.2

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  • COVID-19肺炎との鑑別を要した抗MDA5抗体陽性間質性肺炎の1例

    梁井 由香子, 谷内 七三子, 三宅 絵里佳, 鈴木 彩奈, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 清家 正博, 弦間 昭彦, 吾妻 安良太

    日本内科学会関東地方会   671回   58 - 58   2021.9

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  • 自家骨髄細胞による肺線維症モデルマウスの病態改善効果に関する研究

    神尾 孝一郎, 吾妻 安良太, 松田 久仁子, 猪俣 稔, 久世 眞之, 臼杵 二郎, 田中 徹, 柏田 建, 佐藤 純平, 西島 伸彦, 渥美 健一郎, 齋藤 好信, 清家 正博, 弦間 昭彦

    日本呼吸器学会誌   10 ( 増刊 )   179 - 179   2021.4

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  • COVID-19肺炎との鑑別を要した非HIVニューモシスチス肺炎の1例

    鈴木 彩奈, 谷内 七三子, 佐藤 純平, 西島 伸彦, 神尾 孝一郎, 吾妻 安良太, 清家 正博, 弦間 昭彦

    日本内科学会関東地方会   666回   47 - 47   2021.2

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  • Whole-exome and RNA sequencing reveals chromosomal rearrangements associated with the recurrence of pulmonary carcinoid

    Akihiko Miyanaga, Mari Masuda, Noriko Motoi, Koji Tsuta, Yuka Nakamura, Nobuhiko Nishijima, Shunichi Watanabe, Hisao Asamura, Akihiko Tsuchida, Masahiro Seike, Akihiko Gemma, Tesshi Yamada

    CANCER RESEARCH   80 ( 16 )   2020.8

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    DOI: 10.1158/1538-7445.AM2020-5892

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  • HDAC inhibitorによるXPLNを介するmTORC2-SPARC経路の制御

    神尾 孝一郎, 吾妻 安良太, 臼杵 二郎, 松田 久仁子, 猪俣 稔, 西島 伸彦, 國保 成暁, 板倉 潮人, 山口 朋禎, 藤田 和恵, 齋藤 好信, 阿部 信二, 久保田 馨, 弦間 昭彦

    日本呼吸器学会誌   7 ( 増刊 )   157 - 157   2018.3

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  • HDAC inhibitorによるXPLNを介するmTORC2-SPARC経路の制御

    神尾 孝一郎, 吾妻 安良太, 臼杵 二郎, 松田 久仁子, 猪俣 稔, 西島 伸彦, 國保 成暁, 板倉 潮人, 林 宏紀, 山口 朋禎, 藤田 和恵, 齋藤 好信, 阿部 信二, 久保田 馨, 弦間 昭彦

    分子呼吸器病   22 ( 1 )   111 - 115   2018.3

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    内因性のmTORC2 inhibitorであるExchange factor found in platelets, leukemic and neuronal tissues(XPLN)の作用を通じてmTORC2と肺線維化病態との関連を明らかにし、特発性肺線維症(IPF)の新たな治療戦略を模索することを目的とした。肺線維芽細胞として、human fetal lung fibroblast(HFL-1 cell)を使用した。Small interfering RNA(siRNA)を用いてXPLNをノックダウンし、下流に発現する分子への影響をreal-time PCRとwestern blottingを用いて検討した。またsecreted protein acidic and rich in cysteine(SPARC)の蛍光免疫染色も行った。siRNAによるXPLNのノックダウンによりSPARCの発現が増加し、mTORC2とSPARCとの関連が示された。さらに、HDAC inhibitor(HDACi)であるMS275(entinostat)とSAHA(vorinostat)を用いてHFL-1細胞におけるXPLN発現への影響について検討したところ、両HDACiは濃度依存性にHPLNの発現を有意に増加させた。siRaptorによるXPLNの発現増強はmTORC2活性化に伴いそれを抑制しようとする調節機構と考えられた。

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  • HDAC inhibitorによるXPLNを介するmTORC2-SPARC経路の制御

    神尾 孝一郎, 吾妻 安良太, 臼杵 二郎, 松田 久仁子, 猪俣 稔, 西島 伸彦, 國保 成暁, 板倉 潮人, 林 宏紀, 山口 朋禎, 藤田 和恵, 齋藤 好信, 阿部 信二, 久保田 馨, 弦間 昭彦

    分子呼吸器病   22 ( 1 )   111 - 115   2018.3

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  • HDAC inhibitorによるXPLNを介するmTORC2-SPARC経路の制御

    神尾 孝一郎, 吾妻 安良太, 臼杵 二郎, 松田 久仁子, 猪俣 稔, 西島 伸彦, 國保 成暁, 板倉 潮人, 山口 朋禎, 藤田 和恵, 齋藤 好信, 阿部 信二, 久保田 馨, 弦間 昭彦

    日本呼吸器学会誌   7 ( 増刊 )   157 - 157   2018.3

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  • Xpln Negatively Regulates Sparc Expression By Targeting Mtorc2 In Human Lung Fibroblasts

    K. Kamio, A. Azuma, J. Usuki, K. Matsuda, M. Inomata, N. Nishijima, S. Itakura, N. Kokuho, H. Hayashi, T. Yamaguchi, K. Fujita, Y. Saito, S. Abe, K. Kubota, A. Gemma

    AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE   193   2016

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  • 悪性胸膜中皮腫のペメトレキセド感受性に関与する標的遺伝子の検討

    武内 進, 清家 正博, 野呂 林太郎, 添野 千絵, 西島 伸彦, 松本 優, 峯岸 裕司, 久保田 馨, 弦間 昭彦

    肺癌   53 ( 5 )   680 - 680   2013.10

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  • 小細胞肺癌におけるUGT1A1遺伝子多型の臨床的意義

    峯岸 裕司, 大森 美和子, 渡邉 淳, 西島 伸彦, 松本 優, 宮永 晃彦, 野呂 林太郎, 清家 正博, 島田 隆, 弦間 昭彦

    日本癌治療学会誌   48 ( 3 )   1151 - 1151   2013.9

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  • 胸部悪性腫瘍におけるUGT1A1*28/*6遺伝子多型とイリノテカンの副作用に関する検討

    大森美和子, 峯岸裕司, 渡邊淳, 西島伸彦, 豊川優, 北村和広, 野呂林太郎, 清家正博, 島田隆, 弦間昭彦

    日本呼吸器学会誌   2 ( 増刊 )   168 - 168   2013.3

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  • 非扁平上皮/非小細胞肺癌に対するCarboplatin+Pemetrexed+Bevacizumabの第II相試験

    北村和広, 植松和嗣, 安藤真弘, 西島伸彦, 豊川優, 森山岳, 小齊平聖治, 野呂林太郎, 峯岸裕司, 清家正博, 日野光紀, 宮敏路, 久保田馨, 弦間昭彦

    肺癌   52 ( 5 )   616 - 1277   2012.10

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  • 非扁平上皮/非小細胞肺癌に対するCarboplatin+Pemetrexed+Bevacizumabの第II相試験

    北村 和広, 植松 和嗣, 安藤 真弘, 西島 伸彦, 豊川 優, 森山 岳, 小齊平 聖治, 野呂 林太郎, 峯岸 裕司, 清家 正博, 日野 光紀, 宮 敏路, 久保田 馨, 弦間 昭彦

    日本癌治療学会誌   47 ( 3 )   1277 - 1277   2012.10

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  • 小細胞肺癌に対するmTOR阻害剤の感受性因子・耐性化機序の検討

    豊川 優, 野呂 林太郎, 西島 伸彦, 北村 和広, 小齊平 聖治, 峯岸 裕司, 清家 正博, 添野 千絵, 松田 久仁子, 久保田 馨, 弦間 昭彦

    肺癌   52 ( 5 )   736 - 736   2012.10

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  • 非扁平上皮/非小細胞肺癌に対するCarboplatin + Pemetrexed + Bevacizumabの第II相試験

    北村 和広, 植松 和嗣, 安藤 真弘, 西島 伸彦, 豊川 優, 森山 岳, 小齊平 聖治, 野呂 林太郎, 峯岸 裕司, 清家 正博, 日野 光紀, 宮 敏路, 久保田 馨, 弦間 昭彦

    肺癌   52 ( 5 )   616 - 616   2012.10

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  • 肺癌におけるBIBF1120の治療効果因子の検討(The therapeutic targets of BIBF1120 in lung cancer)

    西島 伸彦, 清家 正博, 添野 千絵, 松田 久仁子, 菅野 哲平, 豊川 優, 北村 和広, 峯岸 裕司, 野呂 林太郎, 吉村 明修, 久保田 馨, 弦間 昭彦

    日本癌学会総会記事   71回   393 - 393   2012.8

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  • 非小細胞癌におけるMET遺伝子FISH陽性はEGFRチロシンキナーゼインヒビターの耐性化の予測因子になりうる(MET FISH positive predicts the resistance to EGFR-TKI in non-small lung cancer patients)

    野呂 林太郎, 清家 正博, 添野 千絵, 西島 伸彦, 松田 久仁子, 菅野 哲平, 豊川 優, 峯岸 裕司, 北村 和広, 吉村 明修, 久保田 馨, 弦間 昭彦

    日本癌学会総会記事   71回   294 - 294   2012.8

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  • 肺癌におけるMET阻害剤の治療標的因子の探索(Search for therapeutic target of MET inhibitor in lung cancer)

    菅野 哲平, 野呂 林太郎, 添野 千恵, 西島 伸彦, 峯岸 裕司, 清家 正博, 弦間 昭彦

    日本癌学会総会記事   71回   335 - 335   2012.8

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  • EGFR遺伝子変異陽性既治療進行肺癌症例に発症した癌性髄膜炎に対してV-Pシャント術とerlotinibの導入にて良好な予後を得た1症例

    坂井 浩佑, 峯岸 裕司, 菅野 哲平, 西島 伸彦, 三浦 由記子, 北村 和広, 小斉平 聖治, 野呂 林太郎, 斉藤 好信, 清家 正博, 吉村 明修, 久保田 馨, 弦間 昭彦

    肺癌   52 ( 3 )   357 - 357   2012.6

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  • 両側肺多発結節影を契機に診断に至ったHIV感染合併histiocytic sarcomaの1例

    成田 宏介, 野呂 林太郎, 豊川 優, 西島 伸彦, 菅野 哲平, 小斉平 聖治, 峯岸 裕司, 清家 正博, 吉村 明修, 久保田 馨, 弦間 昭彦, 高橋 美紀子, 功刀 しのぶ, 川本 雅司, 原田 大, 土屋 眞一

    肺癌   52 ( 2 )   253 - 253   2012.4

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  • FDG-PETによる進行非小細胞肺癌の初回化学療法の効果予測についての検討

    成田 宏介, 清水 久実, 西島 伸彦, 豊川 優, 北村 和広, 小斉平 聖治, 野呂 林太郎, 峯岸 裕司, 清家 正博, 吉村 明修, 久保田 馨, 弦間 昭彦

    日本呼吸器学会誌   1 ( 増刊 )   247 - 247   2012.3

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  • 【肺癌診療の新しい時代】 小細胞肺癌の化学療法

    西島 伸彦, 久保田 馨

    成人病と生活習慣病   42 ( 1 )   77 - 79   2012.1

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    ・小細胞肺癌(SCLC)は限局型(LD)と進展型(ED)に病期分類されるが、ともに併用化学療法が治療の礎石である。・LD-SCLCでは胸部放射線が併用される。・LD-SCLCに対する初回化学療法はシスプラチン+エトポシド、ED-SCLCに対してはシスプラチン+イリノテカンが標準レジメンである。・再発・再燃SCLCの治療(2次化学療法)は、アムルビシンなどの単剤治療が標準である。(著者抄録)

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  • 胸腔ドレナージ・胸膜癒着術難治癌性胸水症例に対するベバシズマブ包含化学療法

    北村和広, 安藤真弘, 高橋聡, 菅野哲平, 西島伸彦, 豊川優, 小齊平聖治, 野呂林太郎, 峯岸裕司, 清家正博, 吉村明修, 弦間昭彦

    肺癌   51 ( 5 )   571 - 571   2011.10

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  • 悪性胸膜中皮腫のペメトレキセド感受性に関与する標的遺伝子とmicroRNAの検討

    武内進, 清家正博, 野呂林太郎, 添野千絵, 成田宏介, 菅野哲平, 西島伸彦, 豊川優, 北村和広, 小齊平聖治, 峯岸裕司, 吉村明修, 弦間昭彦

    肺癌   51 ( 5 )   472 - 472   2011.10

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  • 原発性肺癌におけるUGT1A1*28/*6遺伝子多型と塩酸イリノテカン副作用に関する検討

    峯岸裕司, 渡邉淳, 西島伸彦, 菅野哲平, 豊川優, 小齊平聖治, 野呂林太郎, 清家正博, 吉村明修, 島田隆, 弦間昭彦

    肺癌   51 ( 5 )   549 - 549   2011.10

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  • clear cell differentiationを呈した原発不明癌にBevacizumabが著効した1例

    高橋 聡, 三輪 晃士, 安藤 真弘, 岩波 洋, 北村 和広, 恩田 直美, 菅野 哲平, 西島 伸彦, 武内 進, 豊川 優, 小齊平 聖治, 野呂 林太郎, 峯岸 裕司, 清家 正博, 吉村 明修, 弦間 昭彦, 高橋 美紀子, 川本 雅司, 土屋 眞一

    肺癌   51 ( 6 )   769 - 769   2011.10

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  • clear cell differentiationを呈した原発不明癌にbevacizumabが著効した1例

    高橋聡, 三輪晃士, 安藤真弘, 岩波洋, 北村和広, 恩田直美, 菅野哲平, 西島伸彦, 武内進, 豊川優, 小齊平聖治, 野呂林太郎, 峯岸裕司, 清家正博, 吉村明修, 弦間昭彦, 高橋美紀子, 川本雅司, 土屋眞一

    気管支学   33 ( 5 )   390 - 390   2011.9

  • clear cell differentiationを呈した原発不明癌にBevacizumabが著効した1例

    高橋聡, 北村和広, 恩田直美, 菅野哲平, 西島伸彦, 武内進, 豊川優, 小齊平聖治, 野呂林太郎, 峯岸裕司, 清家正博, 吉村明修, 弦間昭彦, 高橋美紀子, 川本雅司, 土屋眞一

    肺癌   51 ( 4 )   285 - 286   2011.8

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  • 小細胞肺癌に対するmTOR阻害剤の感受性因子の探索

    豊川優, 野呂林太郎, 清家正博, 菅野哲平, 西島伸彦, 武内進, 宮永晃彦, 北村和広, 小齊平聖治, 峯岸裕司, 添野千絵, 松田久仁子, 吉村明修, 弦間昭彦

    肺癌   51 ( 5 )   464 - 464   2011

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  • 高齢者肺癌の臨床背景、治療戦略と予後

    内藤 陽一, 大江 裕一郎, 仁保 誠治, 大松 広伸, 後藤 功一, 葉 清隆, 西島 伸彦, 久保田 馨, 永井 完治, 西脇 裕

    肺癌   50 ( 5 )   555 - 555   2010.10

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  • LUNG CANCER IN NEVER-SMOKERS

    Y. Naito, K. Kubota, Y. Ohe, S. Niho, H. Ohmatsu, K. Goto, K. Yoh, N. Nishijima, K. Nagai, Y. Nishiwaki

    ANNALS OF ONCOLOGY   21   127 - 127   2010.10

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  • 進行扁平上皮癌に対するネダプラチン、ドセタキセル併用療法の第II相試験

    内藤 陽一, 久保田 馨, 大松 広伸, 後藤 功一, 仁保 誠治, 葉 清隆, 釼持 広知, 徳永 裕一, 山根 由紀, 西島 伸彦, 山口 葉子, 太良 哲彦, 伊藤 まさみ, 大江 裕一郎, 西脇 裕

    肺癌   49 ( 5 )   634 - 634   2009.10

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  • 進行肺扁平上皮癌に対するネダプラチン、ドセタキセル併用療法の第I/II相試験

    内藤 陽一, 久保田 馨, 大松 広伸, 後藤 功一, 仁保 誠治, 葉 清隆, 釼持 広知, 徳永 裕一, 永野 達也, 山根 由紀, 西島 伸彦, 山口 葉子, 西條 長宏, 西脇 裕

    日本呼吸器学会雑誌   47 ( 増刊 )   270 - 270   2009.5

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  • 非喫煙者における切除不能非小細胞肺癌の予後の検討

    西島 伸彦, 久保田 馨, 大松 広伸, 後藤 功一, 仁保 誠治, 葉 清隆, 石井 源一郎, 徳永 裕一, 釼持 広知, 永野 達也, 内藤 陽一, 山根 由紀, 山口 葉子, 西條 長宏, 西脇 裕

    日本呼吸器学会雑誌   47 ( 増刊 )   184 - 184   2009.5

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  • 多発脳転移を認めた胸腺腫の1例

    山口 葉子, 葉 清隆, 大松 広伸, 久保田 馨, 後藤 功一, 仁保 誠治, 釼持 広知, 内藤 陽一, 永野 達也, 山根 由紀, 徳永 裕一, 西島 伸彦, 西條 長宏, 西脇 裕, 石井 源一郎

    肺癌   49 ( 1 )   128 - 129   2009.2

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  • 【肺癌診療の進歩】 肺癌化学療法 わが国の標準療法

    西島 伸彦, 久保田 馨

    呼吸と循環   56 ( 12 )   1229 - 1234   2008.12

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    DOI: 10.11477/mf.1404101164

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    Other Link: http://search.jamas.or.jp/link/ui/2009043401

  • 大細胞神経内分泌腫瘍(LCNEC)に対する化学療法の検討

    西島 伸彦, 久保田 馨, 大松 広伸, 後藤 功一, 仁保 誠治, 徳永 祐一, 葉 清隆, 吉本 健太郎, 釼持 広知, 永野 達也, 内藤 陽一, 山根 由紀, 山口 葉子, 西條 長宏, 西脇 裕

    肺癌   48 ( 5 )   647 - 647   2008.10

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  • 小細胞肺癌化学療法における塩酸アムルビシンの血液毒性に関する検討

    山口 葉子, 葉 清隆, 久保田 馨, 大松 広伸, 後藤 功一, 仁保 誠治, 釼持 広知, 内藤 陽一, 永野 達也, 山根 由紀, 徳永 裕一, 西島 伸彦, 西條 長宏, 西脇 裕

    肺癌   48 ( 5 )   465 - 465   2008.10

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  • 骨転移を有する進行非小細胞肺癌に対するゾレドロネート+ドセタキセル+シスプラチン併用療法の第II相試験

    葉 清隆, 久保田 馨, 大松 広伸, 後藤 功一, 仁保 誠治, 釼持 広知, 内藤 陽一, 永野 達也, 山根 由紀, 徳永 裕一, 西島 伸彦, 山口 葉子, 西條 長宏, 西脇 裕

    肺癌   48 ( 5 )   433 - 433   2008.10

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  • ゲフィチニブ耐性肺腺癌に対するエルロチニブの抗腫瘍効果

    内藤 陽一, 後藤 功一, 久保田 馨, 大松 広伸, 仁保 誠治, 葉 清隆, 剱持 広知, 徳永 裕一, 永野 達也, 山根 由紀, 西島 伸彦, 山口 葉子, 西條 長宏, 西脇 裕

    肺癌   48 ( 5 )   421 - 421   2008.10

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  • 著明な気道狭窄を呈した気管癌(腺様嚢胞癌)の1例

    西島 伸彦, 久保田 馨, 大松 広伸, 後藤 功一, 仁保 誠治, 葉 清隆, 徳永 裕一, 吉本 健太郎, 釼持 広知, 永野 達也, 内藤 陽一, 山根 由紀, 山口 葉子, 西條 長宏, 西脇 裕, 石井 源一郎

    肺癌   48 ( 4 )   348 - 348   2008.8

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