FullText URL fulltext.pdf
Author Watanabe, Kenta| Katsui, Kuniaki| Sugiyama, Soichiro| Yoshio, Kotaro| Kuroda, Masahiro| Hiraki, Takao| Kiura, Katsuyuki| Maeda, Yoshinobu| Toyooka, Shinichi| Kanazawa, Susumu|
Keywords Clinical pathology Elderly Non-small cell lung carcinoma Radiosurgery Stereotactic body radiation therapy
Published Date 2021-02-23
Publication Title Radiation Oncology
Volume volume16
Issue issue1
Publisher BMC
Start Page 39
ISSN 1748-717X
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 33622369
DOI 10.1186/s13014-021-01769-7
Web of Science KeyUT 000623175000001
Related Url isVersionOf https://doi.org/10.1186/s13014-021-01769-7
Author Hayakawa, Hiromi| Ichihara, Eiki| Ohashi, Kadoaki| Ninomiya, Takashi| Yasugi, Masayuki| Takata, Saburo| Sakai, Katsuya| Matsumoto, Kunio| Takigawa, Nagio| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-11
Publication Title Cancer Science
Volume volume104
Issue issue11
Content Type Journal Article
FullText URL fulltext.pdf
Author Makimoto, Go| Ohashi, Kadoaki| Taniguchi, Kohei| Soh, Junichi| Taniguchi, Akihiko| Miyahara, Nobuaki| Toyooka, Shinichi| Yoshino, Tadashi| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords IgG4-related disease Pleural effusion Adenosine deaminase Pleural biopsy Spontaneous remission
Published Date 2019
Publication Title Respiratory Medicine Case Reports
Volume volume28
Publisher Elsevier
Start Page 100938
ISSN 2213-0071
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2019 The Authors.
File Version publisher
PubMed ID 31667074
DOI 10.1016/j.rmcr.2019.100938
Web of Science KeyUT 000511444900052
Related Url isVersionOf https://doi.org/10.1016/j.rmcr.2019.100938
Author Rai, Kammei| Takigawa, Nagio| Ito, Sachio| Kashihara, Hiromi| Ichihara, Eiki| Yasuda, Tatsuji| Shimizu, Kenji| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2011-09
Publication Title Molecular Cancer Therapeutics
Volume volume10
Issue issue9
Content Type Journal Article
Author Harada, Daijiro| Takigawa, Nagio| Ochi, Nobuaki| Ninomiya, Takashi| Yasugi, Masayuki| Kubo, Toshio| Takeda, Hiromasa| Ichihara, Eiki| Ohashi, Kadoaki| Takata, Saburo| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2012-10
Publication Title Cancer Science
Volume volume103
Issue issue10
Content Type Journal Article
JaLCDOI 10.18926/AMO/46851
FullText URL 65_4_259.pdf
Author Ogata, Yoshiko| Aoe, Keisuke| Hiraki, Akio| Murakami, Kazuo| Kishino, Daizo| Chikamori, Kenichi| Maeda, Tadashi| Ueoka, Hiroshi| Kiura, Katsuyuki| Tanimoto, Mitsune|
Abstract The objective of this study was to evaluate the utility of the determination of adenosine deaminase (ADA) level in pleural fluid for the differential diagnosis between tuberculous pleural effusion (TPE) and malignant pleural effusion (MPE) in Japan, a country with intermediate incidence of tuberculosis (TB). We retrospectively reviewed the clinical records of 435 patients with pleural effusion and investigated their pleural ADA levels as determined by an auto analyzer. ROC analysis was also performed. The study included patients with MPE (n=188), TPE (n=124), benign nontuberculous pleural effusion (n=94), and pleural effusion of unknown etiology (n=29). The median ADA level in the TPE group was 70.8U/L, which was significantly higher than that in any other groups (p<0.05). The area under the curve (AUC) in ROC analysis was 0.895. With a cut-off level for ADA of 36U/L, the sensitivity, specificity, positive predictive value, and negative predictive value were 85.5%, 86.5%, 69.7%, and 93.6%, respectively. As many as 9% of patients with lung cancer and 15% of those with mesothelioma were false-positive with this ADA cutoff setting. Although the ADA activity in pleural fluid can help in the diagnosis of TPE, it should be noted that some cases of lung cancer or mesothelioma show high ADA activity in geographical regions with intermediate incidence of TB, in contrast to high prevalence areas.
Keywords pleural effusion adenosine deaminase tuberculosis lung cancer mesothelioma
Amo Type Original Article
Published Date 2011-08
Publication Title Acta Medica Okayama
Volume volume65
Issue issue4
Publisher Okayama University Medical School
Start Page 259
End Page 263
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2011 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 21860532
Web of Science KeyUT 000294236700006
JaLCDOI 10.18926/AMO/31590
FullText URL fulltext.pdf
Author Segawa, Yoshihiko| Ohnoshi, Taisuke| Hiraki, Shunkichi| Ueoka, Hiroshi| Kiura, Katsuyuki| Kamei, Haruhito| Tabata, Masahiro| Shibayama, Takuo| Miyatake, Kazuyo| Genda, ken-ichi| Matsumura, Tadashi| Kimura, Ikuro|
Abstract <p>In an attempt to elucidate the tumor properties relating to responsiveness to chemotherapy, we examined immunohistochemically the expression of P-glycoprotein (P-gp) and carcinoembryonic antigen (CEA) in small cell lung cancer (SCLC) tumors. Tumor specimens from 33 patients were obtained at the time of diagnosis and relapse. Four patients expressed P-gp in their initial tumors, and 7 others did in recurrent tumors. The overall response rate to chemotherapy of the initial tumors was 75% for P-gp-positive initial tumors and 86% for P-gp-negative tumors, whereas the disease-free and overall survival times were significantly shorter in the former than the latter. Three patients showed CEA in their initial tumors, and 5 others did in recurrent tumors. The patients with CEA-positive initial tumors tended to relapse earlier than those with CEA-negative tumors. In addition, recurrent tumors expressing CEA were resistant to salvage chemotherapy. A clear correlation between CEA expression by tumors and the CEA level in the serum was observed at diagnosis as well as at relapse. These findings indicate that P-gp and/or CEA expression by a tumor and elevated CEA level in the serum may predict refractoriness of the tumor to chemotherapy.</p>
Keywords small cell lung cancer immunohistochemistry drug resistance P-glycoprotein carcinoembryonic antigen
Amo Type Article
Published Date 1993-06
Publication Title Acta Medica Okayama
Volume volume47
Issue issue3
Publisher Okayama University Medical School
Start Page 181
End Page 189
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 8104371
Web of Science KeyUT A1993LL12400007
Author Kiura, Katsuyuki| Takigawa, Nagio| Oze, Isao| Yasugi, Masayuki| Ochi, Nobuaki| Harada, Daijiro| Tanimoto, Mitsune|
Published Date 2008-01-04
Publication Title 岡山医学会雑誌
Volume volume119
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/54503
FullText URL 70_4_273.pdf
Author Makimoto, Go| Miyahara, Nobuaki| Yoshikawa, Mao| Taniguchi, Akihiko| Kanehiro, Arihiko| Tanimoto, Mitsune| Kiura, Katsuyuki|
Abstract Heerfordtʼs syndrome is a rare manifestation of sarcoidosis and is defined as a combination of facial palsy, parotid swelling, and uveitis, associated with a low-grade fever. We report a case of Heerfordtʼs syndrome presenting with a high fever and increased serum tumor necrosis factor alpha (TNF-α) levels. The patient had facial palsy, parotid swelling, uveitis, and swelling of the right supraclavicular and hilar lymph nodes. Corticosteroid therapy was initiated, and her symptoms soon resolved completely, in tandem with a decrease in TNF-α serum levels.
Keywords Heerfordtʼs syndrome sarcoidosis TNF-α
Amo Type Case Report
Published Date 2016-08
Publication Title Acta Medica Okayama
Volume volume70
Issue issue4
Publisher Okayama University Medical School
Start Page 273
End Page 277
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 27549672
Web of Science KeyUT 000384748600007
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/30795
FullText URL fulltext.pdf
Author Matsuo, Keisuke| Kiura, Katsuyuki| Ueoka, Hiroshi| Tabata, Masahiro| Shibayama, Takuo| Matsumura, Tadashi| Takigawa, Nagio| Hiraki, Shunkichi| Harada, Mine|
Abstract <p>We have established an Adriamycin (ADM) -resistant small cell lung cancer (SCLC) cell line, SBC-3/ADM100, which shows multifactorial mechanisms of resistance to ADM, such as overexpression of P-glycoprotein, an enhanced detoxifying system and a decrease in topoisomerase II activity. In the present study, we confirmed that SBC-3/ADM 100 showed collateral sensitivity to methotrexate and TNP-351, a new antifolate, though this cell line showed a typical multidrug resistance (MDR) pattern. We also demonstrated a faster uptake and higher accumulation (1.3-fold) of TNP-351 in the SBC-3/ADM100 cells than those in the parent SBC-3 cells. These results explain one of the mechanisms for collateral sensitivity in the resistant cells. Furthermore, this cell line was found to have no cross-resistance to edatrexate and minimal cross-resistance to trimetrexate, 254-S (cisplatin analog), 5-fluorouracil and 4-hydroperoxyifosfamide. These drugs will have clinical importance in patients with SCLC who were previously treated with an ADM-containing regimen. Thus, antifolates, especially TNP-351 and edatrexate, can be expected to eradicate residual multidrug resistant SCLC cells selected by ADM.</p>
Keywords Adriamycin-resistant cell line antifolates small cell lung cancer
Amo Type Article
Published Date 1997-06
Publication Title Acta Medica Okayama
Volume volume51
Issue issue3
Publisher Okayama University Medical School
Start Page 121
End Page 127
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 9227790
Web of Science KeyUT A1997XJ12700002
Author Yasugi, Masayuki| Takigawa, Nagio| Ochi, Nobuaki| Ohashi, Kadoaki| Harada, Daijiro| Ninomiya, Takashi| Murakami, Toshi| Honda, Yoshihiro| Ichihara, Eiki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-08-15
Publication Title Experimental Cell Research
Volume volume326
Issue issue2
Content Type Journal Article
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
Author Kiura, Katsuyuki|
Published Date 1993-09-30
Publication Title
Content Type Thesis or Dissertation
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/32669
FullText URL fulltext.pdf
Author Takigawa, Nagio| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro|
Abstract <p>An etoposide-resistant subline, SBC-3/ETP, from a human small cell lung cancer cell line, SBC-3, was developed by continuous exposure to increasing concentrations of etoposide in culture. The SBC-3/ETP was 52.1-fold more resistant to etoposide than the parent cell line. The SBC-3/ETP was highly cross-resistant to teniposide, adriamycin, vinca alkaloids, 4-hydroperoxycyclophosphamide, CPT-11 and mitomycin C, and marginally cross-resistant to cisplatin, while the subline showed a collateral sensitivity to bleomycin. Topoisomerase I activity in the SBC-3/ETP was reduced to an extent of one half and topoisomerase II activity to an extent of one eighth in comparison with those of the SBC-3. Intracellular accumulation of [3H]-etoposide in the SBC-3/ETP was significantly lower in comparison to the SBC-3. An overexpression of MDR1 mRNA, and the presence of its product, P-glycoprotein, were detected in the SBC-3/ETP by Northern blotting and flowcytometry using a monoclonal antibody of the protein, MRK16. These results indicate that a decreased activity of topoisomerase II is the major factor for the development of etoposide resistance, and that an overexpression of the MDR1 gene is responsible, in part, for the development of resistance to the drug and some structurally unrelated compounds such as adriamycin and vinca alkaloids.</p>
Keywords small cell lung cancer etoposide-resistant cell line P-glycoprotein topoisomerase
Amo Type Article
Published Date 1992-06
Publication Title Acta Medica Okayama
Volume volume46
Issue issue3
Publisher Okayama University Medical School
Start Page 203
End Page 212
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 1354408
Web of Science KeyUT A1992JB50400009
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
Author Murakami, Toshi| Takigawa, Nagio| Ninomiya, Takashi| Ochi, Nobuaki| Yasugi, Masaaki| Honda, Yoshihiro| Kubo, Toshio| Ichihara, Eiki| Hotta, Katsuyuki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-01
Publication Title Lung Cancer
Volume volume83
Issue issue1
Content Type Journal Article
Author Rai, Kammei| Takigawa, Nagio| Ito, Sachio| Kashihara, Hiromi| Ichihara, Eiki| Yasuda, Tatsuji| Shimizu, Kenji| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2012-12-03
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue3
Content Type Journal Article
Author Suehisa, Hiroshi| Toyooka, Shinichi| Hotta, Katsuyuki| Uchida, Akiko| Soh, Junichi| Fujiwara, Yoshiro| Matsuo, Keitaro| Ouchida, Mamoru| Takata, Minoru| Kiura, Katsuyuki| Date, Hiroshi|
Published Date 2008-12-01
Publication Title 岡山医学会雑誌
Volume volume120
Issue issue3
Content Type Journal Article