Advance

NONAGASE Yoshikane

    Kindai University Hospital　Assistant Professor B in Medical School
Last Updated :2024/04/25

Researcher Information

J-Global ID

Research Areas

  • Life sciences / Tumor biology

Association Memberships

  • 日本臨床腫瘍学会   THE JAPANESE SOCIETY OF INTERNAL MEDICINE   

Published Papers

  • Yusuke Kawanaka; Yuto Yasuda; Junko Tanizaki; Daisuke Iwashima; Yoshikane Nonagase; Kiyoshi Uemasu; Yutaka Hirayama; Masakazu Ogura; Tomohiro Ozaki; Ken-Ichi Takahashi
    Respiratory investigation 60 (5) 667 - 673 2022/09 
    BACKGROUND: Some lung cancer patients have preexisting interstitial lung disease (ILD), which is considered a risk factor for lung cancer treatment. This study investigated the safety and efficacy of durvalumab consolidation therapy for patients with stage III non-small-cell lung cancer (NSCLC) and preexisting ILD. METHODS: Fifty consecutive patients who were judged to be tolerable to concurrent chemoradiotherapy (CCRT) for stage III NSCLC were enrolled. Differences in the incidence rate of radiation pneumonitis (RP) and progression-free survival (PFS) were assessed in patients with or without ILD of which CT showed non-usual interstitial pneumonia pattern between the durvalumab consolidation group and chemotherapy (combination of carboplatin and paclitaxel [CP]) consolidation group. RESULTS: The incidence of RP was higher in patients with preexisting ILD (40% and 20% in the durvalumab and CP groups, respectively) than in those without ILD (26% and 8% in the durvalumab and CP groups, respectively). Univariate analysis showed that durvalumab therapy tended to increase the incidence of RP; however, preexisting ILD did not significantly increase the incidence of RP. The condition of all patients who developed RP improved with the administration of oral prednisolone. Among patients without ILD, the median PFS was 17 and 16 months in the durvalumab and CP groups, respectively. Among patients with preexisting ILD, median PFS was not achieved in the durvalumab group and was 8 months in the CP group. CONCLUSIONS: Although durvalumab consolidation therapy tended to increase the incidence of RP, it might be tolerable in stage III NSCLC patients with preexisting ILD.
  • がん悪液質患者に対するアナモレリン塩酸塩の臨床的検討
    中山 智裕; 渡邉 諭美; 野長瀬 祥兼; 尾崎 智博
    日本内科学会雑誌 (一社)日本内科学会 111 (臨増) 221 - 221 0021-5384 2022/02
  • Ryoji Kato; Hidetoshi Hayashi; Kazuko Sakai; Shinichiro Suzuki; Koji Haratani; Takayuki Takahama; Junko Tanizaki; Yoshikane Nonagase; Kaoru Tanaka; Takeshi Yoshida; Masayuki Takeda; Kimio Yonesaka; Hiroyasu Kaneda; Kazuto Nishio; Kazuhiko Nakagawa
    International Journal of Clinical Oncology Springer Science and Business Media LLC 1341-9625 2021/06
  • Masayuki Takeda; Takayuki Takahama; Kazuko Sakai; Shigeki Shimizu; Satomi Watanabe; Hisato Kawakami; Kaoru Tanaka; Chihiro Sato; Hidetoshi Hayashi; Yoshikane Nonagase; Kimio Yonesaka; Naoki Takegawa; Tatsuya Okuno; Takeshi Yoshida; Soichi Fumita; Shinichiro Suzuki; Koji Haratani; Kazumasa Saigoh; Akihiko Ito; Tetsuya Mitsudomi; Hisashi Handa; Kazuya Fukuoka; Kazuhiko Nakagawa; Kazuto Nishio
    The oncologist 26 (4) e588-e596  2021/04 
    BACKGROUND: Implementation of personalized medicine requires the accessibility of tumor molecular profiling in order to allow prioritization of appropriate targeted therapies for individual patients. Our aim was to study the role of comprehensive genomic profiling assays that may inform treatment recommendations for patients with solid tumors. MATERIALS AND METHODS: We performed a prospective study to evaluate the feasibility of application of the FoundationOne CDx panel-which detects substitutions, insertions and deletions, and copy number alterations in 324 genes, select gene rearrangements, and genomic signatures including microsatellite instability and tumor mutation burden (TMB)-to patients with advanced or recurrent solid tumors before its approval in Japan. RESULTS: A total of 181 samples were processed for genomic testing between September 2018 and June 2019, with data being successfully obtained for 175 of these samples, yielding a success rate of 96.7%. The median turnaround time was 41 days (range, 21-126 days). The most common known or likely pathogenic variants were TP53 mutations (n = 113), PIK3CA mutations (n = 33), APC mutations (n = 32), and KRAS mutations (n = 29). Among the 153 patients assessed for TMB, the median TMB was 4 mutations/Mb, and tumors with a high TMB (≥10 mutations/Mb) were more prevalent for lung cancer (11/32) than for other solid tumor types (9/121, Fisher's exact test p < .01). No clear trend toward increased efficacy for immune checkpoint inhibitor (ICI) monotherapy or ICI combination chemotherapy in patients with a high programmed cell death-ligand 1 tumor proportion score or a high TMB was apparent. Among the 174 patients found to harbor known or likely pathogenic actionable alterations, 24 individuals (14%) received matched targeted therapy. CONCLUSION: The FoundationOne CDx assay was performed with formalin-fixed, paraffin-embedded tumor specimens with a success rate of >95%. Such testing may inform the matching of patients with cancer with investigational or approved targeted drugs. IMPLICATIONS FOR PRACTICE: This prospective cohort study was initiated to investigate the feasibility and utility of clinical application of FoundationOne CDx. A total of 181 samples were processed for genomic testing between September 2018 and June 2019, with data being successfully obtained for 175 of these samples, yielding a success rate of 96.7%, and 24 individuals (14%) received matched targeted therapy.
  • 加藤 了資; 林 秀敏; 原谷 浩司; 高濱 隆幸; 谷崎 潤子; 野長瀬 祥兼; 田中 薫; 吉田 健史; 武田 真幸; 米阪 仁雄; 中川 和彦; 坂井 和子; 西尾 和人; 金田 裕靖
    肺癌 (NPO)日本肺癌学会 60 (2) 148 - 148 0386-9628 2020/04
  • CAPP-Seqを用いたLiquid biopsyによるT790M陽性非小細胞肺癌のオシメルチニブ耐性因子の検討
    加藤 了資; 林 秀敏; 原谷 浩司; 高濱 隆幸; 谷崎 潤子; 野長瀬 祥兼; 田中 薫; 吉田 健史; 武田 真幸; 米阪 仁雄; 中川 和彦; 坂井 和子; 西尾 和人; 金田 裕靖
    肺癌 (NPO)日本肺癌学会 60 (2) 148 - 148 0386-9628 2020/04
  • TAKASHI KUROSAKI; HISATO KAWAKAMI; SEIICHIRO MITANI; RYOHEI KAWABATA; TAKAYUKI TAKAHAMA; YOSHIKANE NONAGASE; SOICHI FUMITA; TOMOHIRO OZAKI; YASUTAKA CHIBA; TAKAO TAMURA; KAZUHIKO NAKAGAWA
    In Vivo Anticancer Research USA Inc. 34 (4) 1921 - 1929 0258-851X 2020
  • 田中 薫; 谷崎 潤子; 野長瀬 祥兼; 原谷 浩司; 酒井 瞳; 加藤 了資; 渡邉 諭美; 吉田 健史; 佐藤 千尋; 林 秀敏; 坂井 和子; 西尾 和人; 中川 和彦
    肺癌 (NPO)日本肺癌学会 59 (6) 694 - 694 0386-9628 2019/11
  • 野長瀬 祥兼; 武田 真幸; 東 公一; 林 秀敏; 原谷 浩司; 田中 薫; 米阪 仁雄; 石井 秀宜; 星野 友昭; 中川 和彦
    肺癌 (NPO)日本肺癌学会 59 (6) 765 - 765 0386-9628 2019/11
  • Yoshikane Nonagase; Masayuki Takeda; Koichi Azuma; Hidetoshi Hayashi; Koji Haratani; Kaoru Tanaka; Kimio Yonesaka; Hidenobu Ishii; Tomoaki Hoshino; Kazuhiko Nakagawa
    Thoracic cancer 10 (10) 1928 - 1935 2019/10 [Refereed]
     
    BACKGROUND: Non-small cell lung cancer (NSCLC) positive for activating mutations of the epidermal growth factor receptor (EGFR) gene is initially sensitive to EGFR-tyrosine kinase inhibitors (TKIs) but eventually develops resistance to these drugs. Upregulation of the receptor tyrosine kinase AXL in tumor tissue has been detected in about one-fifth of NSCLC patients with acquired resistance to EGFR-TKIs. However, the clinical relevance of the levels of AXL and its ligand GAS6 in plasma remains unknown. METHODS: Tumor tissue and plasma specimens were collected from 25 EGFR-mutated NSCLC patients before EGFR-TKI treatment or after treatment failure. The levels of AXL and of GAS6 mRNA in tumor tissue were evaluated by immunohistochemistry and chromogenic in situ hybridization, respectively. The plasma concentrations of AXL and GAS6 were measured with enzyme-linked immunosorbent assays. RESULTS: AXL expression was detected in three of 12 (25%) and nine of 19 (47%) tumor specimens obtained before and after EGFR-TKI treatment, respectively. All tumor specimens assayed were positive for GAS6 mRNA. The median values for the plasma AXL concentration before and after EGFR TKI treatment were 1 635 and 1 460 pg/mL, respectively, and those for the plasma GAS6 concentration were 4 615 and 6 390 pg./mL, respectively. There was no significant correlation between the plasma levels of AXL or GAS6 and the corresponding expression levels in tumor tissue. CONCLUSION: Plasma concentrations of AXL and GAS6 do not reflect tumor expression levels, and their measurement is thus not a viable alternative to direct analysis of tumor tissue in EGFR-mutated NSCLC.
  • Sakai K; Takeda M; Shimizu S; Takahama T; Yoshida T; Watanabe S; Iwasa T; Yonesaka K; Suzuki S; Hayashi H; Kawakami H; Nonagase Y; Tanaka K; Tsurutani J; Saigoh K; Ito A; Mitsudomi T; Nakagawa K; Nishio K
    Scientific reports 9 (1) 11340  2019/08 [Refereed]
  • Naoki Takegawa; Junji Tsurutani; Hisato Kawakami; Kimio Yonesaka; Ryoji Kato; Koji Haratani; Hidetoshi Hayashi; Masayuki Takeda; Yoshikane Nonagase; Osamu Maenishi; Kazuhiko Nakagawa
    International Journal of Cancer Wiley 2019/05 [Refereed]
  • Watanabe S; Yonesaka K; Tanizaki J; Nonagase Y; Takegawa N; Haratani K; Kawakami H; Hayashi H; Takeda M; Tsurutani J; Nakagawa K
    Cancer Med 8 (1258) 1268  2019 [Refereed]
  • Ueda H; Kawakami H; Nonagase Y; Takegawa N; Okuno T; Takahama T; Takeda M; Chiba Y; Tamura T; Nakagawa K
    Oncotarget 24 (2) 163  2019 [Refereed]
  • Nonagase Y; Takeda M; Tanaka K; Hayashi H; Iwasa T; Nakagawa K
    Oncotarget. 9 (50) 29532 - 29535 2018/06 [Refereed]
     
    © Nonagase et al. Malignant tumors can induce a hypercoagulable state known as Trousseau syndrome that increases the risk for venous thromboembolism including disabling cerebral infarction. Anticoagulant therapy without anticancer treatment is not effective for amelioration of this coagulation abnormality. Most patients with lung cancer positive for activating mutations of the epidermal growth factor receptor (EGFR) are sensitive to EGFR tyrosine kinase inhibitors (TKIs), but the efficacy and safety of EGFR-TKIs in such patients with a poor performance status (PS) due to Trousseau syndrome has been unclear. We here describe a patient with EGFR mutation-positive lung cancer who developed disabling cerebral infarction due to Trousseau syndrome. Administration of the EGFR-TKI gefitinib and anticoagulant therapy resulted in a partial tumor response and recovery from both the coagulation abnormality and the severe neurological symptoms. After the development of resistance to gefitinib, the EGFR-TKI osimertinib was safely administered until disease progression without recurrence of the coagulation abnormality. This case suggests that gefitinib followed by osimertinib may be a safe and effective treatment option for patients with EGFR mutation-positive lung cancer who experience disabling cerebral infarction due to Trousseau syndrome.
  • 悪性リンパ腫放射線治療後、2次発癌として進行食道癌を併発した1例
    奥野 達哉; 植田 勲人; 武川 直樹; 野長瀬 祥兼; 川上 尚人; 谷崎 潤子; 林 秀敏; 田中 薫; 武田 真幸; 鶴谷 純司; 中川 和彦
    日本消化器病学会雑誌 (一財)日本消化器病学会 115 (臨増総会) A328 - A328 0446-6586 2018/03
  • Naoki Takegawa; Yoshikane Nonagase; Kimio Yonesaka; Kazuko Sakai; Osamu Maenishi; Yusuke Ogitani; Takao Tamura; Kazuto Nishio; Kazuhiko Nakagawa; Junji Tsurutani
    INTERNATIONAL JOURNAL OF CANCER WILEY 141 (8) 1682 - 1689 0020-7136 2017/10 [Refereed]
     
    Anti-HER2 therapies are beneficial for patients with HER2-positive breast or gastric cancer. T-DM1 is a HER2-targeting antibody-drug conjugate (ADC) comprising the antibody trastuzumab, a linker, and the tubulin inhibitor DM1. Although effective in treating advanced breast cancer, all patients eventually develop T-DM1 resistance. DS-8201a is a new ADC incorporating an anti-HER2 antibody, a newly developed, enzymatically cleavable peptide linker, and a novel, potent, exatecan-derivative topoisomerase I inhibitor (DXd). DS-8201a has a drug-to-antibody-ratio (DAR) of 8, which is higher than that of T-DM1 (3.5). Owing to these unique characteristics and unlike T-DM1, DS-8201a is effective against cancers with low-HER2 expression. In the present work, T-DM1-resistant cells (N87-TDMR), established using the HER2-positive gastric cancer line NCI-N87 and continuous T-DM1 exposure, were shown to be susceptible to DS-8201a. The ATP-binding cassette (ABC) transporters ABCC2 and ABCG2 were upregulated in N87-TDMR cells, but HER2 overexpression was retained. Furthermore, inhibition of ABCC2 and ABCG2 by MK571 restored T-DM1 sensitivity. Therefore, resistance to T-DM1 is caused by efflux of its payload DM1, due to aberrant expression of ABC transporters. In contrast to DM1, DXd payload of DS-8201a inhibited the growth of N87-TDMR cells in vitro. This suggests that either DXd may be a poor substrate of ABCC2 and ABCG2 in comparison to DM1, or the high DAR of DS8201a relative to T-DM1 compensates for increased efflux. Notably, N87-TDMR xenograft tumor growth was prevented by DS8201a. In conclusion, the efficacy of DS-8201a as a treatment for patients with T-DM1-resistant breast or gastric cancer merits investigation.
  • K. Haratani; H. Hayashi; T. Tanaka; H. Kaneda; Y. Togashi; K. Sakai; K. Hayashi; S. Tomida; Y. Chiba; K. Yonesaka; Y. Nonagase; T. Takahama; J. Tanizaki; K. Tanaka; T. Yoshida; K. Tanimura; M. Takeda; H. Yoshioka; T. Ishida; T. Mitsudomi; K. Nishio; K. Nakagawa
    ANNALS OF ONCOLOGY OXFORD UNIV PRESS 28 (7) 1532 - 1539 0923-7534 2017/07 [Refereed]
     
    Background: The efficacy of programmed death-1 blockade in epidermal growth factor receptor gene (EGFR) mutation-positive non-small-cell lung cancer (NSCLC) patients with different mechanisms of acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) is unknown. We retrospectively evaluated nivolumab efficacy and immune-related factors in such patients according to their status for the T790M resistance mutation of EGFR. Patients and methods: We identified 25 patients with EGFR mutation-positive NSCLC who were treated with nivolumab after disease progression during EGFR-TKI treatment (cohort A). Programmed death-ligand 1 (PD-L1) expression and tumor-infiltrating lymphocyte (TIL) density in tumor specimens obtained after acquisition of EGFR-TKI resistance were determined by immunohistochemistry. Whole-exome sequencing of tumor DNA was carried out to identify gene alterations. The relation of T790M status to PD-L1 expression or TIL density was also examined in an independent cohort of 60 patients (cohort B). Results: In cohort A, median progression-free survival (PFS) was 2.1 and 1.3 months for T790M-negative and T790M-positive patients, respectively (P = 0.099; hazard ratio of 0.48 with a 95% confidence interval of 0.20-1.24). Median PFS was 2.1 and 1.3 months for patients with a PD-L1 expression level of >= 1% or <1%, respectively (P = 0.084; hazard ratio of 0.37, 95% confidence interval of 0.10-1.21). PFS tended to increase as the PD-L1 expression level increased with cutoff values of >= 10% and >= 50%. The proportion of tumors with a PD-L1 level of >= 10% or >= 50% was higher among T790M-negative patients than among T790M-positive patients of both cohorts A and B. Nivolumab responders had a significantly higher CD8(+) TIL density and nonsynonymous mutation burden. Conclusion: T790M-negative patients with EGFR mutation-positive NSCLC are more likely to benefit from nivolumab after EGFR-TKI treatment, possibly as a result of a higher PD-L1 expression level, than are T790M-positive patients.
  • Yoshikane Nonagase; Kimio Yonesaka; Hisato Kawakami; Satomi Watanabe; Koji Haratani; Takayuki Takahama; Naoki Takegawa; Hiroto Ueda; Junko Tanizaki; Hidetoshi Hayashi; Takeshi Yoshida; Masayuki Takeda; Yasutaka Chiba; Takao Tamura; Kazuhiko Nakagawa; Junji Tsurutani
    ONCOTARGET IMPACT JOURNALS LLC 7 (51) 84860 - 84871 1949-2553 2016/12 [Refereed]
     
    Background: Overexpression of heregulin, a HER3 ligand, is one mechanism that confers resistance to the anti-HER2 agents trastuzumab and lapatinib. We investigated the impact of heregulin expression on the efficacy of HER2-targeted therapeutic agents, including trastuzumab, trastuzumab emtansine (T-DM1) and lapatinib, in vitro and in vivo and evaluated the heregulin messenger RNA (mRNA) levels in specimens from patients with HER2-positive breast or gastric cancer. Results: Cell proliferation and apoptosis assays demonstrated that heregulin conferred robust resistance to lapatinib and trastuzumab via HER3-Akt pathway activation followed by survivin overexpression; however, heregulin conferred minimal or no resistance to T-DM1 and paclitaxel. The heregulin mRNA level of one of 10 patients was up-regulated after the acquisition of resistance to trastuzumab-based therapy. Materials and Methods: SK-BR-3, NCI-N87, BT-474, MDA-MB-453, HCC1954, SNU-216 and 4-1ST cells were pharmacologically treated with recombinant heregulin or transfected with the heregulin gene. We also assessed the expression of heregulin mRNA in HER2-positive breast or gastric cancer samples before and after trastuzumab-based therapy using a RT-PCR-based method. Conclusions: mRNA up-regulation of heregulin was observed in clinical breast cancer specimens during trastuzumab-based treatment, but heregulin overexpression had a limited effect on the sensitivity to T-DM1 in vitro and in vivo.
  • Yoshikane Nonagase; Kunio Okamoto; Tsutomu Iwasa; Takeshi Yoshida; Kaoru Tanaka; Masayuki Takeda; Hiroyasu Kaneda; Toshio Shimizu; Junji Tsurutani; Kazuhiko Nakagawa
    ANTI-CANCER DRUGS LIPPINCOTT WILLIAMS & WILKINS 27 (3) 251 - 253 0959-4973 2016/03 [Refereed]
     
    Both afatinib and erlotinib are tyrosine kinase inhibitors that inhibit aberrant epidermal growth factor receptor (EGFR) signals in non-small-cell lung cancer (NSCLC). Afatinib is an irreversible inhibitor directed against EGFR, ErbB-2, and ErbB-4, whereas erlotinib is a reversible inhibitor directed against EGFR only. Although afatinib has been shown to be effective in the treatment for erlotinib-refractory and/or gefitinib-refractory central nervous system metastases from NSCLC, little is known about the efficacy of erlotinib for afatinib-refractory central nervous system metastases. In the present report we describe a case of EGFR mutation-positive NSCLC in which brain metastases developed during first-line afatinib treatment. Whole-brain radiation therapy and substitution of erlotinib for afatinib led to successful shrinkage of the brain metastases. Our report highlights the potential benefit of erlotinib for the management of brain metastases refractory over afatinib in patients with NSCLC.
  • Naoki Takegawa; Kimio Yonesaka; Kazuko Sakai; Hiroto Ueda; Satomi Watanabe; Yoshikane Nonagase; Tatsuya Okuno; Masayuki Takeda; Osamu Maenishi; Junji Tsurutani; Taroh Satoh; Isamu Okamoto; Kazuto Nishio; Takao Tamura; Kazuhiko Nakagawa
    ONCOTARGET IMPACT JOURNALS LLC 7 (3) 3443 - 3450 1949-2553 2016/01 [Refereed]
     
    Background: Patients with metastatic colorectal cancer (mCRC) harboring wild-type KRAS benefit from epidermal growth factor receptor (EGFR)-targeted therapy. However, patients who are treated with anti-EGFR antibodies will eventually develop the resistance to those agents. HER2 amplification is one of the mechanisms conferring resistance to anti-EGFR antibody therapy and could therefore be a potential therapeutic target. The aim of this study was to detect HER2 amplification in circulating tumor DNA (ctDNA) from patients with CRC and acquired resistance to anti-EGFR antibody therapy Results: Our data showed that 22% (4/18) of patients in the cohort exhibited HER2 amplification. One of these patients was found to be positive for HER2 amplification in matched tumor specimens collected after cetuximab therapy, at which point the patient had acquired cetuximab resistance, despite being negative for HER2 amplification prior to therapy. Methods: We analyzed plasma ctDNA using digital polymerase chain reaction (PCR) from 18 patients with CRC, who had been treated with anti-EGFR antibody-based therapy (cetuximab) and subsequently acquired resistant cetuximab. HER2 gene copy number was analyzed using fluorescence in situ hybridization in tumor samples before and after acquisition of resistance to cetuximab-based therapy. Conclusion: Analysis of plasma ctDNA by digital PCR could be useful for detecting HER2 amplification in patients with CRC who were resistant to anti-EGFR antibody therapy.
  • M. Takeda; K. Sakai; M. Terashima; H. Kaneda; H. Hayashi; K. Tanaka; K. Okamoto; T. Takahama; T. Yoshida; T. Iwasa; T. Shimizu; Y. Nonagase; K. Kudo; S. Tomida; T. Mitsudomi; K. Saigo; A. Ito; K. Nakagawa; K. Nishio
    ANNALS OF ONCOLOGY OXFORD UNIV PRESS 26 (12) 2477 - 2482 0923-7534 2015/12 [Refereed]
     
    The clinical implementation of genomic profiling for lung cancer with high-throughput, multiplex tests is warranted to allow prioritization of appropriate therapies for individual patients. Multiplex genomic testing can assist physicians in matching patients with approved or experimental targeted treatments. Background: The clinical implementation of genomic profiling for lung cancer with high-throughput, multiplex tests is warranted to allow prioritization of appropriate therapies for individual patients. We have now applied such testing to detect actionable mutations that may inform treatment recommendations in lung cancer. Patients and methods: We prospectively applied amplicon sequencing panels that cover both mutational hotspots in 22 genes related to lung and colon tumorigenesis as well as 72 major variants of ALK, RET, ROS1, and NTRK1 fusion transcripts. We then determined the proportion of patients who received genotype-directed therapy and their overall survival (OS). Results: Tumor specimens from 110 patients with lung cancer recruited between July 2013 and March 2015 were analyzed. The most common genetic alterations were TP53 mutations in 42 patients, followed by EGFR mutations in 25, STK11 mutations in 12, and KRAS mutations in 10. Potentially actionable mutations were identified in 44 patients including 50% of those with adenocarcinoma and 14% of those with squamous cell carcinoma. The OS of patients with advanced or recurrent cancer who had an actionable mutation and received targeted therapy (median OS not achieved) was significantly longer than that of those with no mutation (18.1 months, P = 0.041) or of those with a mutation not so treated (6.1 months, P = 0.0027). Conclusions: Multiplex genomic testing was performed on formalin-fixed, paraffin-embedded tumor specimens with a success rate of >= 95%. Such testing can assist physicians in matching patients with approved or experimental targeted treatments. Clinical trial registration: The University Medical Hospital Information Network (UMIN) Clinical Trials Registry under the identifier UMIN000014782.
  • Shinya Ueda; Hisato Kawakami; Shinichi Nishina; Tsutomu Sakiyama; Yoshikane Nonagase; Takafumi Okabe; Takao Tamura; Kazuhiko Nakagawa
    CANCER CHEMOTHERAPY AND PHARMACOLOGY SPRINGER 76 (2) 279 - 285 0344-5704 2015/08 [Refereed]
     
    Purpose The aims of this dose-escalating phase I study were to determine the maximum tolerable dose (MTD) and recommended dose (RD) of 5-fluorouracil (5-FU), docetaxel, and nedaplatin (UDON) combination therapy for future phase II studies, and to evaluate the safety and efficacy of this regimen in patients with untreated recurrent or metastatic esophageal cancer. Methods Patients were administered 5-FU on days 1-5, docetaxel on days 1 and 15, and nedaplatin on day 1 at 4-week intervals. The dose levels of 5-FU/docetaxel/nedaplatin were escalated as follows (mg/m(2)): level 1, 800/30/80; level 2, 800/30/90; and level 3, 800/35/90. Toxicity was evaluated using Common Terminology Criteria for Adverse Events version 4.0. Results Overall, nine patients were enrolled in this study. All patients had an Eastern Cooperative Oncology Group performance status of 0 or 1 and were diagnosed with squamous cell carcinoma. No dose-limiting toxicity was observed at any level, and planned dose escalation was completed without reaching the MTD. No grade 4 or higher toxicity was observed in this study. The observed grade 3 hematological toxicities included neutropenia in five patients (55.6 %) and leukopenia in three patients (33.3 %). None of the patients developed febrile neutropenia, and no grade 3 or 4 non-hematological toxicities were observed. The overall response rate was 77.8 %, including two complete responses, and the disease control rate was 100 %. Conclusion The RD of UDON was identified as level 3. The good tolerability and high antitumor efficacy of this regimen warrant further evaluation in this setting.
  • T. Sakiyama; J. Tsurutani; T. Iwasa; H. Kawakami; Y. Nonagase; T. Yoshida; K. Tanaka; Y. Fujisaka; T. Kurata; Y. Komoike; K. Nishio; K. Nakagawa
    BRITISH JOURNAL OF CANCER NATURE PUBLISHING GROUP 112 (5) 819 - 824 0007-0920 2015/03 [Refereed]
     
    Background: We evaluated the safety, maximum-tolerated dose (MTD), pharmacokinetics, recommended dose for phase II (P2RD), and preliminary anticancer activity of a combination eribulin and S-1 therapeutic in metastatic breast cancer patients pretreated with anthracycline and taxane. Method: Patients aged 20-74 years were recruited. In level 1, patients received S-1 (65mgm(-2)) from day 1 to 14, and eribulin (1.1mgm(-2)) on day 1 and 8 in a 21-day cycle. In level 2, eribulin was increased to 1.4mgm(-2). In level 3, S-1 was increased to 80 mgm(-2). Results: Twelve patients were enrolled into three cohorts. Planned dose escalation was completed, with one case exhibiting doselimiting toxicity (grade 3 hypokalaemia) at level 3, without reaching the MTD. The P2RD was determined to be level 2 (eribulin 1.4mgm(-2) and S-1 65mgm(-2)). The most common grade 3 or 4 toxicity was neutropenia (83.3%), followed by febrile neutropenia (25.0%). Five of eleven patients (41.7%) with measurable disease had a partial response. Pharmacokinetics were characterised by dose-dependent elimination and nonlinear exposure. Conclusion: Dose level 3 was not tolerated owing to febrile neutropenia development. Thus, intermediate dose level 2 was recommended for further evaluation. Preliminary antitumour activity warrants further investigation in this setting.
  • Tsutomu Iwasa; Tsutomu Sakiyama; Junji Tsurutani; Kaoru Tanaka; Takeshi Yoshida; Yoshikane Nonagase; Yasuhito Fujisaka; Takayasu Kurata; Yoshifumi Komoike; Kazuhiko Nakagawa
    ANNALS OF ONCOLOGY OXFORD UNIV PRESS 25 0923-7534 2014/10 [Refereed]

MISC

  • 加藤了資; 林秀敏; 原谷浩司; 高濱隆幸; 谷崎潤子; 野長瀬祥兼; 田中薫; 吉田健史; 武田真幸; 米阪仁雄; 中川和彦; 坂井和子; 西尾和人; 高濱隆幸; 谷崎潤子; 野長瀬祥兼; 金田裕靖  肺癌(Web)  60-  (2)  2020
  • 野長瀬 祥兼; 武田 真幸; 東 公一; 林 秀敏; 原谷 浩司; 田中 薫; 米阪 仁雄; 石井 秀宜; 星野 友昭; 中川 和彦  肺癌  59-  (6)  765  -765  2019/11
  • ALK融合遺伝子陽性非小細胞肺癌におけるALK-TKI耐性機序に関する検討
    田中 薫; 谷崎 潤子; 野長瀬 祥兼; 原谷 浩司; 酒井 瞳; 加藤 了資; 渡邉 諭美; 吉田 健史; 佐藤 千尋; 林 秀敏; 坂井 和子; 西尾 和人; 中川 和彦  肺癌  59-  (6)  694  -694  2019/11
  • 悪性リンパ腫放射線治療後、2次発癌として進行食道癌を併発した1例
    奥野 達哉; 武川 直樹; 野長瀬 祥兼; 川上 尚人; 林 秀敏; 中川 和彦  日本食道学会学術集会プログラム・抄録集  73回-  258  -258  2019/06
  • ALK融合遺伝子陽性非小細胞肺癌におけるALK-TKI耐性機序に関する検討
    田中 薫; 谷崎 潤子; 野長瀬 祥兼; 原谷 浩司; 酒井 瞳; 林 秀敏; 中川 和彦; 坂井 和子; 西尾 和人  肺癌  58-  (5)  373  -373  2018/10
  • ALK融合遺伝子陽性非小細胞肺癌におけるALK-TKI耐性機序に関する検討
    田中 薫; 谷崎 潤子; 野長瀬 祥兼; 原谷 浩司; 酒井 瞳; 林 秀敏; 坂井 和子; 西尾 和人; 中川 和彦  肺癌  58-  (6)  691  -691  2018/10
  • 悪性リンパ腫放射線治療後、2次発癌として進行食道癌を併発した1例
    奥野 達哉; 植田 勲人; 武川 直樹; 野長瀬 祥兼; 川上 尚人; 谷崎 潤子; 林 秀敏; 田中 薫; 武田 真幸; 鶴谷 純司; 中川 和彦  日本消化器病学会雑誌  115-  (臨増総会)  A328  -A328  2018/04
  • Satoru Iwasa; Kohei Shitara; Shunji Takahashi; Haeseong Park; Shigenori Kadowaki; Shanu Modi; Yoshikane Nonagase; Kenji Tamura; Kensei Yamaguchi; Kei Muro; Junji Tsurutani; Javad Shahidi; Caleb C. Lee; Masahiro Sugihara; Yoshinori Kawaguchi; Toshihiko Doi  JOURNAL OF CLINICAL ONCOLOGY  36-  (4)  2018/02
  • 田中薫; 谷崎潤子; 野長瀬祥兼; 原谷浩司; 酒井瞳; 林秀敏; 中川和彦; 坂井和子; 西尾和人  肺癌(Web)  58-  (5)  2018
  • 野長瀬 祥兼; 米阪 仁雄; 川上 尚人; 渡邉 諭美; 原谷 浩司; 高濱 隆幸; 武川 直樹; 植田 勲人; 谷崎 潤子; 林 秀俊; 吉田 健史; 武田 真幸; 千葉 康敬; 中川 和彦; 鶴谷 純司  近畿大学医学雑誌 = Medical Journal of Kindai University  42-  (3)  25A1  -25A1  2017/12
  • Trousseau症候群とDICを合併した肺腺癌にgefitinibが奏功した1例
    野長瀬 祥兼; 武田 真幸; 田中 薫; 吉田 健史; 林 秀敏; 中川 和彦  肺癌  57-  (7)  879  -879  2017/12
  • Yoshikane Nonagase; Naoki Takegawa; Kimio Yonesaka; Kazuko Sakai; Yusuke Ogitani; Junji Tsurutani; Kazuto Nishio; Kazuhiko Nakagawa  CANCER RESEARCH  77-  2017/07
  • セツキシマブ耐性の大腸癌患者における血漿におけるHER2遺伝子増幅の検出
    武川 直樹; 米阪 仁雄; 坂井 和子; 野長瀬 祥兼; 植田 勲人; 奥野 達哉; 前西 修; 川上 尚人; 鶴谷 純司; 田村 孝雄; 中川 和彦  日本消化器病学会雑誌  114-  (臨増総会)  A297  -A297  2017/03
  • セツキシマブ耐性の大腸癌患者における血漿におけるHER2遺伝子増幅の検出
    武川 直樹; 米阪 仁雄; 坂井 和子; 野長瀬 祥兼; 植田 勲人; 奥野 達哉; 前西 修; 川上 尚人; 鶴谷 純司; 田村 孝雄; 中川 和彦  日本消化器病学会雑誌  114-  (臨増総会)  A297  -A297  2017/03
  • 高濱隆幸; 武田真幸; 清水俊雄; 坂井和子; 田中薫; 野長瀬祥兼; 原谷浩司; 鶴谷純司; 西尾和人; 中川和彦  日本臨床腫瘍学会学術集会(CD-ROM)  15th-  ROMBUNNO.O1‐2‐6  2017
  • 肺癌に於ける次世代シーケンサーを用いた変異解析に基づく分子標的薬適応決定
    武田 真幸; 坂井 和子; 林 秀敏; 田中 薫; 吉田 健史; 岩朝 勤; 高濱 隆幸; 野長瀬 祥兼; 西尾 和人; 中川 和彦  近畿大学医学雑誌  41-  (3-4)  19A  -19A  2016/12
  • 肺癌に於ける次世代シーケンサーを用いた変異解析に基づく分子標的薬適応決定
    武田 真幸; 坂井 和子; 林 秀敏; 田中 薫; 吉田 健史; 岩朝 勤; 高濱 隆幸; 野長瀬 祥兼; 西尾 和人; 中川 和彦  近畿大学医学雑誌  41-  (3-4)  19A  -19A  2016/12
  • 武田真幸; 坂井和子; 林秀敏; 田中薫; 吉田健史; 岩朝勤; 高濱隆幸; 野長瀬祥兼; 西尾和人; 中川和彦  日本肺癌学会総会号  57th-  (6)  637  -637  2016/11
  • 肺癌に於ける次世代シーケンサーを用いた変異解析に基づく分子標的薬適応決定
    武田 真幸; 坂井 和子; 林 秀敏; 田中 薫; 吉田 健史; 岩朝 勤; 高濱 隆幸; 野長瀬 祥兼; 西尾 和人; 中川 和彦  肺癌  56-  (6)  637  -637  2016/11
  • Yoshikane Nonagase; Kimio Yonesaka; Satomi Watanabe; Koji Haratani; Takayuki Takahama; Naoki Takegawa; Hiroto Ueda; Hisato Kawakami; Hidetoshi Hayashi; Masayuki Takeda; Haruka Sakamoto; Takao Tamura; Kazuhiko Nakagawa; Junji Tsurutani  CANCER RESEARCH  76-  2016/07
  • Afatinib抵抗性の脳転移を有するEGFR変異陽性進行非小細胞肺癌に対して全脳照射後にErlotinibが長期奏効した1例
    野長瀬 祥兼; 渡邉 諭美; 原谷 浩司; 高濱 隆幸; 武川 直樹; 植田 勲人; 田村 孝雄; 中川 和彦; 岡本 邦男  肺癌  56-  (2)  138  -138  2016/04
  • 野長瀬祥兼; 米阪仁雄; 渡邉諭美; 武川直樹; 川上尚人; 林秀敏; 武田真幸; 田村孝雄; 中川和彦; 鶴谷純司  日本臨床腫瘍学会学術集会(CD-ROM)  14th-  2016
  • 野長瀬祥兼; 渡邉諭美; 原谷浩司; 高濱隆幸; 武川直樹; 植田勲人; 田村孝雄; 中川和彦; 岡本邦男  肺癌(Web)  56-  (2)  138(J‐STAGE)  2016
  • 奥野達哉; 野長瀬祥兼; 武川直樹; 植田勲人; 田中薫; 林秀敏; 武田真幸; 清水俊雄; 鶴谷純司; 田村孝雄; 中川和彦  日本臨床腫瘍学会学術集会(CD-ROM)  14th-  ROMBUNNO.PF1‐084  2016
  • 田中薫; 西田諭美; 原谷浩司; 野長瀬祥兼; 高濱隆幸; 吉田健史; 岩朝勤; 林秀敏; 武田真幸; 金田裕靖; 中川和彦  日本肺癌学会総会号  56th-  (5)  547  -547  2015/10
  • Afatinib抵抗性の脳転移を有するEGFR変異陽性進行非小細胞肺癌に対してErlotinibが長期奏効した一例
    野長瀬 祥兼; 岡本 邦男; 西田 諭美; 原谷 浩司; 高濱 隆幸; 武川 直樹; 植田 勲人; 田村 孝雄; 中川 和彦  肺癌  55-  (5)  486  -486  2015/10
  • Afatinib抵抗性の脳転移を有するEGFR変異陽性進行非小細胞肺癌に対してErlotinibが長期奏効した一例
    野長瀬 祥兼; 岡本 邦男; 西田 諭美; 原谷 浩司; 高濱 隆幸; 武川 直樹; 植田 勲人; 田村 孝雄; 中川 和彦  肺癌  55-  (5)  486  -486  2015/10
  • 田中 薫; 西田 諭美; 原谷 浩司; 野長瀬 祥兼; 高濱 隆幸; 吉田 健史; 岩朝 勤; 林 秀敏; 武田 真幸; 金田 裕靖; 中川 和彦  気管支学 : 日本気管支研究会雑誌  37-  (5)  2015/09
  • 田中 薫; 西田 諭美; 原谷 浩司; 野長瀬 祥兼; 高濱 隆幸; 吉田 健史; 岩朝 勤; 林 秀敏; 武田 真幸; 金田 裕靖; 中川 和彦  気管支学  37-  (5)  607  -607  2015/09
  • 当院における非小細胞肺癌に対するre-biopsyの検討
    田中 薫; 西田 諭美; 原谷 浩司; 野長瀬 祥兼; 高濱 隆幸; 吉田 健史; 岩朝 勤; 林 秀敏; 武田 真幸; 中川 和彦; 金田 裕靖  肺癌  55-  (4)  306  -307  2015/08
  • 非小細胞肺癌 基礎研究 肺癌に於ける次世代シーケンサーを用いた変異解析に基づく分子標的薬適応決定
    武田 真幸; 坂井 和子; 田中 薫; 吉田 健史; 岩朝 勤; 高濱 隆幸; 野長瀬 祥兼; 岡部 崇記; 林 秀敏; 岡本 邦男; 金田 裕靖; 清水 俊雄; 西尾 和人; 中川 和彦  日本呼吸器学会誌  4-  (増刊)  146  -146  2015/03
  • 宮川知保; 田中薫; 西田諭美; 野長瀬祥兼; 高濱隆幸; 吉田健史; 岩朝勤; 工藤慶太; 武田真幸; 金田裕靖; 鶴谷純司; 中川和彦  気管支学  37-  (1)  114  -115  2015/01
  • 副腎転移巣の破裂、出血により急激な全身状態悪化を来した原発性肺扁平上皮癌の一例
    中田 有紀; 高濱 隆幸; 田中 薫; 植田 勲人; 西田 論美; 武川 直樹; 野長瀬 祥兼; 工藤 慶太; 岩朝 勤; 吉田 健史; 武田 真幸; 金田 裕靖; 清水 俊雄; 鶴谷 純司; 田村 孝雄; 中川 和彦  肺癌  54-  (5)  506  -506  2014/10
  • 化学療法中に間質性肺炎増悪を来した肺癌患者転帰の後ろ向き検討
    高濱 隆幸; 金田 裕靖; 田中 薫; 植田 勲人; 西田 諭美; 武川 直樹; 野長瀬 祥兼; 工藤 慶太; 岩朝 勤; 吉田 健史; 武田 真幸; 清水 俊雄; 鶴谷 純司; 田村 孝雄; 中川 和彦  肺癌  54-  (5)  587  -587  2014/10
  • 肺癌に於ける次世代シーケンサーを用いた変異解析に基づく分子標的薬適応決定
    武田 真幸; 清水 俊雄; 田中 薫; 吉田 健史; 岩朝 勤; 高濱 隆幸; 野長瀬 祥兼; 岡部 崇記; 林 秀敏; 岡本 邦男; 坂井 和子; 西尾 和人; 中川 和彦  肺癌  54-  (5)  364  -364  2014/10
  • TAKAHAMA TAKAYUKI; NONAGASE YOSHIKANE; NAKAGAWA KAZUHIKO  分子呼吸器病  18-  (1)  130  -135  2014/03
  • 仁科慎一; 上田眞也; 野長瀬祥兼; 岡部崇記; 崎山努; 川上尚人; 田村孝雄; 中川和彦  日本臨床腫瘍学会学術集会(CD-ROM)  12th-  ROMBUNNO.P2-5-4  2014
  • 高濱隆幸; 野長瀬祥兼; 崎山勉; 川上尚人; 仁科慎一; 田村孝雄; 中川和彦  日本臨床腫瘍学会学術集会(CD-ROM)  12th-  ROMBUNNO.P2-12-6  2014
  • 野長瀬祥兼; 崎山勉; 高濱隆幸; 川上尚人; 仁科慎一; 田村孝雄; 中川和彦  日本臨床腫瘍学会学術集会(CD-ROM)  12th-  ROMBUNNO.P1-30-2  2014
  • 野長瀬祥兼; 崎山勉; 川上尚人; 松岡弘道; 田村孝雄; 小山敦子; 中川和彦  日本サイコオンコロジー学会総会プログラム・抄録集  26th-  137  2013
  • 鶴谷純司; 松岡弘道; 牧村ちひろ; 野長瀬祥兼; 岡本邦男; 田中薫; 仁科慎一; 清水俊雄; 小山敦子; 中川和彦  日本サイコオンコロジー学会総会プログラム・抄録集  26th-  144  2013

Other link

researchmap


Copyright © MEDIA FUSION Co.,Ltd. All rights reserved.