JaLCDOI 10.18926/AMO/31598
FullText URL fulltext.pdf
Author Kiura, Katsuyuki| Ohnoshi, Taisuke| Tabata, Masahiro| Shibayama, Takuo| Kimura, Ikuro|
Abstract A subline highly resistant to Adriamycin (SBC-3/ADM100) was isolated in vitro from the human small cell lung cancer cell line, SBC-3, by culturing in progressively higher concentrations of Adriamycin. The SBC-3/ADM100 cells were 106-fold more resistant to the drug than the parent cells in an inhibitory concentration of 50% determined by the MTT assay. The population-doubling time was much longer in SBC-3/ADM100 than in the parent cells. Northern blot hybridization revealed marked overexpression of the MDR1 mRNA in the resistant cells. P-glycoprotein overexpression and a decrease in intracellular accumulation of Adriamycin were demonstrated in SBC-3/ADM100, indicating that outward drug transport was the major mechanism of resistance in this subline. Additionally, a significant elevation of the intracellular glutathione content coupled with the glutathione S-transferase (GST) pi level and a decrease in DNA topoisomerase II (Topo II) activity were noted in this resistant subline. These results indicate that the mechanism of resistance to Adriamycin is multifactorial; involving altered growth characteristics, an enhanced outward transport, enhanced drug detoxification process, and decreased target enzyme activity. The resistant subline will serve as a useful tool in the search for ways to overcome drug resistance.
Keywords Adriamycin-resistant cell line MDR1 mRNA glutathione glutathione S-transferasse π DNA topoisomerase II
Amo Type Article
Published Date 1993-06
Publication Title Acta Medica Okayama
Volume volume47
Issue issue3
Publisher Okayama University Medical School
Start Page 191
End Page 197
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders Copyright © 1999 Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 8104372
Web of Science KeyUT A1993LL12400008
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/6296
JaLCDOI 10.18926/AMO/31626
FullText URL fulltext.pdf
Author Matsushita, Akio| Tabata, Masahiro| Ueoka, Hiroshi| Kiura, Katsuyuki| Shibayama, Takuo| Aoe, Keisuke| Kohara, Hiroyuki| Harada, Mine|
Abstract <p>We established a drug sensitivity panel consisting of 24 human lung cancer cell lines. Using this panel, we evaluated 26 anti-cancer agents: three alkylators, three platinum compounds, four antimetabolites, one topoisomerase I inhibitor, five topoisomerase II inhibitors, seven antimitotic agents and three tyrosine kinase inhibitors. This panel showed the following: a) Drug sensitivity patterns reflected their clinically-established patterns of action. For example, doxorubicin and etoposide were shown to be active against small cell lung cancer cell lines and mitomycin-C and 5-fluorouracil were active against non-small cell lung cancer cell lines, in agreement with clinical data. b) Correlation analysis of the mean graphs derived from the logarithm of IC50 values of the drugs gave insight into the mechanism of each drug's action. Thus, two drug combinations with reverse or no correlation, such as the combination of cisplatin and vinorelbine, might be good candidates for the ideal two drug combination in the treatment of lung cancer, as is being confirmed in clinical trials. c) Using cluster analysis of the cell lines in the panel with their drug sensitivity patterns, we could classify the cell lines into four groups depending on the drug sensitivity similarity. This classification will be useful to elucidate the cellular mechanism of action and drug resistance. Thus, our drug sensitivity panel will be helpful to explore new drugs or to develop a new combination of anti-cancer agents for the treatment of lung cancer.</p>
Keywords drug screening system MTT assay lung cancer cell line drug resistance
Amo Type Article
Published Date 1999-04
Publication Title Acta Medica Okayama
Volume volume53
Issue issue2
Publisher Okayama University Medical School
Start Page 67
End Page 75
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
Web of Science KeyUT 000080058700002
JaLCDOI 10.18926/AMO/31705
FullText URL fulltext.pdf
Author Takata, Ichiro| Ueoka, Hiroshi| Kiura, Katsuyuki| Tabata, Masahiro| Takigawa, Nagio| Katayama, Hideki| Takemoto, Mitsuhiro| Hiraki, Yoshio| Harada, Mine| Tanimoto, Mitsune|
Abstract <p>A pilot study was conducted to assess the efficacy and feasibility of daily low-dose cisplatin with concurrent thoracic irradiation for clinically unresectable non-small-cell lung cancer (NSCLC). Patients with inoperable NSCLC who had poor risk factors such as advanced age, poor performance status, poor lung function, or concomitant active malignancy were entered into the study. Low-dose cisplatin (6 mg/m2) was administered daily before concurrent thoracic irradiation (2 Gy/day; total dose of 60 Gy) was given. Twenty-five patients were registered. The majority of the patients had either stage IIIA (24.0%) or stage IIIB (60.0%) disease. Fifteen patients (60.0%) completed the planned treatment. Both chemotherapy and radiotherapy were stopped in 3 patients (12.0%) due to poor response, and 7 patients (28.0%) partly received radiotherapy alone as a result of their toxicity response. The proportion of total administered dose to planned dose was 90.9% for chemotherapy and 99.3% for radiotherapy, which were comparable to those in previous studies for LA-NSCLC patients without poor risk factors. Grade 3 leukopenia and neutropenia developed in 14 patients (56.0%) and 10 patients (40.0%), respectively, but grade 4 toxicity was not encountered. Grade 3 pneumonitis and esophagitis were observed in 4 patients (16.0%) and 2 patients (8.0%), respectively. The overall response rate was 60.0%. The median survival time was 22 months, and the 2-year survival rate was 50.3%. Daily low-dose cisplatin and concurrent thoracic irradiation were well tolerated even by poor-risk patients with NSCLC, and showed a therapeutic efficacy similar to that for good-risk patients.</p>
Keywords non-small-cell lung cancer concurrent chemoradiotherapy low-dose cisplatin poor-risk factor
Amo Type Article
Published Date 2002-10
Publication Title Acta Medica Okayama
Volume volume56
Issue issue5
Publisher Okayama University Medical School
Start Page 261
End Page 266
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12530510
Web of Science KeyUT 000178668100007
JaLCDOI 10.18926/AMO/31714
FullText URL fulltext.pdf
Author Kawada, Kazuhiko| Yonei, Toshiro| Ueoka, Hiroshi| Kiura, Katsuyuki| Tabata, Masahiro| Takigawa, Nagio| Harada, Mine| Tanimoto, Mitsune|
Abstract <p>When the development of chemotherapeutic agents reaches the clinical trial stage, it is necessary to perform drug sensitivity tests quickly in order to select the most promising agents for the treatment of cancer. In order to assess the possibility of using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay as a substitute for the human tumor clonogenic assay (HTCA), we evaluated the correlation between the results obtained by these 2 assays in 5 human lung cancer cell lines. The correlation coefficient between the results of the HTCA and the MTT assay was 0.673, indicating a relatively good correlation. The correlation was most prominent in platinum analogues (r = 0.939) and good in anthracyclines/anthracenedione (r = 0.611). However, no significant correlation was observed in vinca alkaloids, etoposide, irinotecan, SN-38 (an active metabolite of irinotecan), and rhizoxin. The results of the MTT assay showed a high degree of correlation with those of the HTCA in predicting the sensitivity of cancer cell lines to platinum analogues, and anthracyclines/anthracenedione. These results suggest that the MTT assay may be more convenient and quickly performed than the HTCA and can replace HTCA in evaluating the effects of anticancer agents, especially the platinum analogues and anthracyclines/anthracenedione.</p>
Keywords chemosensitivity test 3-(4 5-dimethylthiazol-2-yl)-2 5-diphenyltertrazolium bromide (MTT) assay clonogenic assay
Amo Type Article
Published Date 2002-06
Publication Title Acta Medica Okayama
Volume volume56
Issue issue3
Publisher Okayama University Medical School
Start Page 129
End Page 134
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 12108583
Web of Science KeyUT 000176521200002
JaLCDOI 10.18926/AMO/32866
FullText URL fulltext.pdf
Author Fujimoto, Nobukazu| Kiura, Katsuyuki| Takigawa, Nagio| Fujiwara, Yoshiro| Toyooka, Shinichi| Umemura, Shigeki| Tabata, Masahiro| Ueoka, Hiroshi| Tanimoto, Mitsune|
Abstract <p>We examined the feasibility of triplet chemotherapy using cisplatin, docetaxel, and irinotecan for patients with recurrent or refractory non-small cell lung cancer (NSCLC), retrospectively. Twenty-five patients (21 men and 4 women) with NSCLC and good performance status who were &#60;70 years old were analyzed. The median age was 58 years. Most patients had performance status 1 (16/25), stage IV disease (18/25) and adenocarcinoma-histology (16/25). Cisplatin and docetaxel were given on day 1 and irinotecan on day 2;the cycle was repeated every 3 weeks. The objective response rate was 39.1% (95% confidence interval:18.7-59.5%). The median survival time and actual 2-, 3-, and 5-year survival rates were 14.3 months, 32%, 20%, and 8%, respectively. Of note, only 6 patients were treated with gefitinib at the recurrence after triplet chemotherapy;of these, 4 (67%) achieved a partial response, which might result in favorable survival. Grade 3/4 toxicities consisted of neutropenia (100%), neutropenic fever (56%), nausea/vomiting (40%), and diarrhea (16%);no cases of treatment-related death occurred. Triplet chemotherapy showed impressive survival data in our clinical trial, but proved too toxic for use in treating patients with NSCLC in the clinical practice.</p>
Keywords cisplatin docetaxel irinotecan triplet chemotherapy gefitinib
Amo Type Original Article
Published Date 2010-02
Publication Title Acta Medica Okayama
Volume volume64
Issue issue1
Publisher Okayama University Medical School
Start Page 33
End Page 37
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 20200582
Web of Science KeyUT 000274868300005
Title Alternative A prospective cohort study to define the clinical and pathological features of lung cancers harboring HER2 gene aberrations (the HER2-CS Study) and a phase II study of trastuzumab emtansine (recombinant) in patients with HER2-positive non-small cell lung cancer who recurred, progressed after standard chemotherapy, or were primarily refractory to standard chemotherapy
FullText URL 127_127.pdf
Author Kiura, Katsuyuki| Hotta, Katsuyuki| Sato, Akiko| Ohashi, Kadoaki| Ninomiya, Takashi| Minnami, Daisuke| Tabata, Masahiro| Kubo, Toshio| Kato, Yuka| Hirata, Taizo|
Keywords 臨床研究中核病院 国立研究開発法人日本医療研究開発機構 文部科学省橋渡し研究加速ネットワークプログラム HER2-CS study trastuzumab emtansine
Publication Title 岡山医学会雑誌
Published Date 2015-08-03
Volume volume127
Issue issue2
Start Page 127
End Page 132
ISSN 0030-1558
Related Url isVersionOf https://doi.org/10.4044/joma.127.127
language 日本語
Copyright Holders Copyright (c) 2015 岡山医学会
File Version publisher
DOI 10.4044/joma.127.127
NAID 130005096256
JaLCDOI 10.18926/AMO/54499
FullText URL 70_4_243.pdf
Author Osawa, Masahiro| Ohashi, Kadoaki| Kubo, Toshio| Ichihara, Eiki| Takata, Saburo| Takigawa, Nagio| Takata , Minoru| Tanimoto, Mitsune| Kiura, Katsuyuki|
Abstract Vandetanib (ZactimaTM) is a novel, orally available inhibitor of both vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR) tyrosine kinase. In the present study, a line of transgenic mice with a mouse Egfr gene mutation (delE748-A752) corresponding to a human EGFR mutation (delE746-A750) was established. The transgenic mice developed atypical adenomatous hyperplasia to adenocarcinoma of the lung at around 5 weeks of age and died of lung tumors at approximately 17 weeks of age. In the mice treated with vandetanib (6mg/kg/day), these lung tumors disappeared and the phosphorylations of EGFR and VEGFR-2 were reduced in lung tissues to levels comparable to those of non-transgenic control mice. The median overall survival time of the transgenic mice was 28 weeks in the vandetanib-treated group and 17 weeks in the vehicle-treated group. Vandetanib significantly prolonged the survival of the transgenic mice (log-rank test, p<0.01); resistance to vandetanib occurred at 20 weeks of age and the animals died from their lung tumors at about 28 weeks of age. These data suggest that vandetanib could suppress the progression of tumors harboring an activating EGFR mutation.
Keywords vandetanib VEGFR EGFR nonsmall cell lung cancer transgenic mouse
Amo Type Original Article
Published Date 2016-08
Publication Title Acta Medica Okayama
Volume volume70
Issue issue4
Publisher Okayama University Medical School
Start Page 243
End Page 253
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2016 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 27549668
Web of Science KeyUT 000384748600003
FullText URL J_Thorac_Oncol_201907017.pdf
Author Makimoto, Go| Ohashi, Kadoaki| Tomida, Shuta| Nishii, Kazuya| Matsubara, Takehiro| Kayatani, Hiroe| Higo, Hisao| Ninomiya, Kiichiro| Sato, Akiko| Watanabe, Hiromi| Kano, Hirohisa| Ninomiya, Takashi| Kubo, Toshio| Rai, Kammei| Ichihara, Eiki| Hotta, Katsuyuki| Tabata, Masahiro| Toyooka, Shinichi| Takata, Minoru| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords ALK G1202R Alectinib Amphiregulin MET NSCLC
Published Date 2019-07-30
Publication Title Journal of Thoracic Oncology
Volume volume14
Issue issue11
Publisher Elsevier
Start Page 2009
End Page 2018
ISSN 15560864
NCID AA12058455
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2019 International Association for the Study of Lung Cancer. Published by Elsevier Inc. All rights reserved.
File Version author
PubMed ID 31374369
DOI 10.1016/j.jtho.2019.07.017
Web of Science KeyUT 000492678300025
Related Url isVersionOf https://doi.org/10.1016/j.jtho.2019.07.017
FullText URL fulltext.pdf
Author Nishii, Kazuya| Ohashi, Kadoaki| Tamura, Tomoki| Ninomiya, Kiichiro| Matsubara, Takehiro| Senoo, Satoru| Kano, Hirohisa| Watanabe, Hiromi| Oda, Naohiro| Makimoto, Go| Higo, Hisao| Kato, Yuka| Ninomiya, Takashi| Kubo, Toshio| Yamamoto, Hiromasa | Tomida, Shuta| Hotta, Katsuyuki| Tabata, Masahiro| Toyooka, Shinichi| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords non-small cell lung cancer epidermal growth factor receptor mutations droplet digital PCR exhaled breath condensate EGFR-TKIs
Published Date 2020-12
Publication Title Oncology Letters
Volume volume20
Issue issue6
Publisher Spandidos Publications
Start Page 393
ISSN 1792-1074
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version publisher
PubMed ID 33193853
DOI 10.3892/ol.2020.12256
Web of Science KeyUT 000595649300005
Related Url isVersionOf https://doi.org/10.3892/ol.2020.12256
FullText URL fulltext.pdf
Author Watanabe, Hiromi| Ichihara, Eiki| Kayatani, Hiroe| Makimoto, Go| Ninomiya, Kiichiro| Nishii, Kazuya| Higo, Hisao| Ando, Chihiro| Okawa, Sachi| Nakasuka, Takamasa| Kano, Hirohisa| Hara, Naofumi| Hirabae, Atsuko| Kato, Yuka| Ninomiya, Takashi| Kubo, Toshio| Rai, Kammei| Ohashi, Kadoaki| Hotta, Katsuyuki| Tabata, Masahiro| Maeda, Yoshinobu| Kiura, Katsuyuki|
Published Date 2021-01-07
Publication Title Cancer science
Publisher Wiley
ISSN 1347-9032
NCID AA11808050
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2021 The Authors.
File Version publisher
PubMed ID 33410241
NAID 120007008532
DOI 10.1111/cas.14801
Web of Science KeyUT 000630136900001
Related Url isVersionOf https://doi.org/10.1111/cas.14801
FullText URL fulltext.pdf
Author Katsui, Kuniaki| Ogata, Takeshi| Sugiyama, Soichi| Yoshio, Kotaro| Kuroda, Masahiro| Hiraki, Takao| Kiura, Katsuyuki| Maeda, Yoshinobu| Toyooka, Shinichi| Kanazawa, Susumu|
Published Date 2021-06-04
Publication Title scientific reports
Volume volume11
Issue issue1
Publisher Nature Research
Start Page 11882
ISSN 2045-2322
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © The Author(s) 2021
File Version publisher
PubMed ID 34088965
DOI 10.1038/s41598-021-91449-z
Web of Science KeyUT 000678611200010
Related Url isVersionOf https://doi.org/10.1038/s41598-021-91449-z
Author Nishii, Kazuya| Ohashi, Kadoaki| Watanabe, Hiromi| Makimoto, Go| Nakasuka, Takamasa| Higo, Hisao| Ninomiya, Kiichiro| Kato, Yuka| Kubo, Toshio| Rai, Kammei| Ichihara, Eiki| Hotta, Katsuyuki| Tabata, Masahiro| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords epidermal growth factor receptor osimertinib bevacizumab cetuximab hypoxia‑inducible factor‑1α transforming growth factor‑α
Note This is an open access article distributed under the terms of Creative Commons Attribution License.|
Published Date 2021-7-7
Publication Title Oncology Letters
Volume volume22
Issue issue3
Publisher Spandidos Publications
Start Page 639
ISSN 1792-1074
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © Nishii et al.
File Version publisher
DOI 10.3892/ol.2021.12900
Web of Science KeyUT 000678494600001
Related Url isVersionOf https://doi.org/10.3892/ol.2021.12900
FullText URL fulltext.pdf
Author Okawa, Sachi| Rai, Kammei| Fujii, Nobuharu| Gion, Yuka| Ninomiya, Kiichiro| Kato, Yuka| Taniguchi, Akihiko| Kubo, Toshio| Ichihara, Eiki| Ohashi, Kadoaki| Miyahara, Nobuaki| Hotta, Katsuyuki| Tabata, Masahiro| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords EGFR IgG4-related disease marginal zone lymphoma osimertinib
Published Date 2021-09-01
Publication Title Internal Medicine
Volume volume60
Issue issue17
Publisher The Japanese Society of Internal Medicine
Start Page 2831
End Page 2837
ISSN 0918-2918
NCID AA10827774
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2021 The Japanese Society of Internal Medicine
File Version publisher
PubMed ID 33775999
DOI 10.2169/internalmedicine.6470-20
Web of Science KeyUT 000695856000020
Related Url isVersionOf https://doi.org/10.2169/internalmedicine.6470-20
FullText URL fulltext.pdf
Author Oda, Naohiro| Tabata, Masahiro| Uno, Masatoshi| Umeda, Yuzo| Kato, Hironari| Kubo, Toshio| Senoo, Satoru| Yagi, Takahito| Fujiwara, Toshiyoshi| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords pancreas mucinous cystadenocarcinoma carboplatin paclitaxel
Published Date 2021-09-15
Publication Title Internal Medicine
Volume volume60
Issue issue18
Publisher The Japanese Society of Internal Medicine
Start Page 2967
End Page 2971
ISSN 0918-2918
NCID AA10827774
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2021 The Japanese Society of Internal Medicine
File Version publisher
PubMed ID 33814494
DOI 10.2169/internalmedicine.6730-20
Web of Science KeyUT 000697279400013
Related Url isVersionOf https://doi.org/10.2169/internalmedicine.6730-20