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/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
JaLCDOI 10.18926/AMO/40503
FullText URL 64_5_285.pdf
Author Nishimori, Hisakazu| Takahashi, Shunji| Kiura, Katsuyuki| Ennishi, Daisuke| Kobayashi, Takayuki| Sano, Koji| Shinozaki, Eiji| Yokoyama, Masahiro| Mishima, Yuko| Terui, Yasuhito| Chin, Keisho| Mizunuma, Nobuyuki| Ito, Yoshinori| Nishimura, Seiichiro| Takeuchi, Kengo| Ishikawa, Yuichi| Oguchi, Masahiko| Tanimoto, Mitsune| Hatake, Kiyohiko|
Abstract We evaluated the efficacy and toxicity of cisplatin/docetaxel (CDDP/TXT) chemotherapy and identified prognostic factors in Japanese patients with cancer of unknown primary site (CUP). Twenty-eight consecutive patients seen at a single institute were reviewed retrospectively. Sixteen patients were treated with TXT 80mg/m2, followed by CDDP 75mg/m2. The overall response rate to CDDP/TXT treatment was 62.5%, with a median survival time (MST) of 22.7 months. Common adverse reactions were myelosuppression and hyponatremia. The MST of all 28 patients with CUP was 8.3 months, and the 1-year overall survival rate was 45.6%. Univariate analysis identified 5 prognostic factors:performance status, liver involvement, bone involvement, pleural involvement, and lymph node involvement. In conclusion, CDDP/TXT chemotherapy is effective with tolerable toxicity in patients with CUP. Japanese patients with CUP might be chemosensitive and may survive longer.
Keywords cancer of unknown primary site (CUP) cisplatin docetaxel prognosis
Amo Type Original Article
Published Date 2010-10
Publication Title Acta Medica Okayama
Volume volume64
Issue issue5
Publisher Okayama University Medical School
Start Page 285
End Page 291
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2010 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 20975761
Web of Science KeyUT 000283563300003
Author Ichihara, Eiki| Ohashi, Kadoaki| Takigawa, Nagio| Osawa, Masahiro| Ogino, Atsuko| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2011-04-01
Publication Title 岡山医学会雑誌
Volume volume123
Issue issue1
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
Author Nogami, Naoyuki| Hotta, Katsuyuki| Kuyama, Shoichi| Kiura, Katsuyuki| Takigawa, Nagio| Chikamori, Kenichi| Shibayama, Takuo| Kishino, Daizo| Hosokawa, Shinobu| Tamaoki, Akihiko| Harita, Shingo| Tabata, Masahiro| Ueoka, Hiroshi| Shinkai, Tetsu| Tanimoto, Mitsune|
Published Date 2011-10
Publication Title Lung Cancer
Volume volume74
Issue issue1
Content Type Journal Article
Author Taniguchi, Akihiko| Miyahara, Nobuaki| Nakahara, Atsushi| Takata, Saburo| Sakugawa, Ryo| Nagano, Osamu| Tanimoto, Yasushi| Kanehiro, Arihiko| Kiura, Katsuyuki| Ujike, Yoshito| Tanimoto, Mitsune|
Published Date 2011-12-01
Publication Title 岡山医学会雑誌
Volume volume123
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/47260
FullText URL 65_6_353.pdf
Author Ichihara, Eiki| Kiura, Katsuyuki| Tanimoto, Mitsune|
Abstract Angiogenesis is an essential process in tumor growth. The concept of angiogenesis, when proposed by Folksman in 1971, had a great impact on cancer research and therapy, as the survival and proliferation of cancer depend on angiogenesis, which could be a target of cancer therapy. In subsequent decades, numerous antiangiogenic agents were developed, and some of them have been applied clinically. However, angiogenesis includes a complex and multistep process that has not been sufficiently elucidated. In this review, we focus on signaling pathways related with tumor angiogenesis and several antiangiogenic agents approved by the United States Food and Drug Administration or under investigation.
Keywords angiogenesis cancer
Amo Type Review
Published Date 2011-12
Publication Title Acta Medica Okayama
Volume volume65
Issue issue6
Publisher Okayama University Medical School
Start Page 353
End Page 362
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 22189475
Web of Science KeyUT 000298516900001
JaLCDOI 10.18926/AMO/48564
FullText URL 66_3_245.pdf
Author Okada, Toshiaki| Takigawa, Nagio| Kishino, Daizo| Katayama, Hideki| Kuyama, Shouichi| Sato, Ken| Mimoto, Junko| Ueoka, Hiroshi| Tanimoto, Mitsune| Kiura, Katsuyuki|
Abstract Cisplatin is used to treat lung cancer;however, it is also a known carcinogen. Cyclooxygenase-2 (COX-2) inhibitors have been shown to prevent carcinogen-induced experimental tumors. We investigated the effect of a COX-2 inhibitor, celecoxib, on cisplatin-induced lung tumors. One hundred twenty 4-week-old A/J mice were divided into 6 groups:group 1, no treatment;group 2, low-dose celecoxib (150mg/kg);group 3, high-dose celecoxib (1,500mg/kg);group 4, cisplatin alone;group 5, cisplatin plus low-dose celecoxib;and group 6, cisplatin plus high-dose celecoxib. Mice in groups 4-6 were administered cisplatin (1.62mg/kg, i.p.) once a week for 10 weeks between 7 and 16 weeks of age. All mice were sacrificed at week 30. Tumor incidence was 15.8% in group 1, 25% in group 2, 26.3% in group 3, 60% in group 4, 50% in group 5, and 50% in group 6. Tumor multiplicity was 0.2, 0.3, 0.3, 1.3, 1.0, and 0.6 in groups 1-6, respectively. Tumor multiplicity in the cisplatin-treated mice was reduced by celecoxib treatment in a dose-dependent manner (p<0.05, group 4 vs. group 6). Celecoxib significantly reduced COX-2 expression in cisplatin-induced tumors (p<0.01, group 4 vs. group 6).
Keywords cisplatin non-small cell lung cancer celecoxib cyclooxygenase-2 chemoprevention
Amo Type Original Article
Published Date 2012-06
Publication Title Acta Medica Okayama
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 245
End Page 251
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22729105
Web of Science KeyUT 000305669700008
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 Kiura, Katsuyuki| Tanimoto, Mitsune|
Published Date 2013-04-01
Publication Title 岡山医学会雑誌
Volume volume125
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 2011-09
Publication Title Molecular Cancer Therapeutics
Volume volume10
Issue issue9
Content Type Journal Article
Author Kubo, Toshio| Takigawa, Nagio| Osawa, Masahiro| Harada, Daijiro| Ninomiya, Takashi| Ochi, Nobuaki| Ichihara, Eiki| Yamane, Hiromichi| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-01
Publication Title Cancer Science
Volume volume104
Issue issue1
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
Author Shien, Kazuhiko| Toyooka, Shinichi| Ichimura, Kouichi| Soh, Junichi| Furukawa, Masashi| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Ueno, Tsuyoshi| Asano, Hiroaki| Tsukuda, Kazunori| Yamane, Masaomi| Oto, Takahiro| Kiura, Katsuyuki| Miyoshi, Shinichiro|
Published Date 2012-07
Publication Title Lung Cancer
Volume volume77
Issue issue1
Content Type Journal Article
Author Ueno, Tsuyoshi| Tsukuda, Kazunori| Toyooka, Shinichi| Ando, Midori| Takaoka, Munenori| Soh, Junichi| Asano, Hiroaki| Maki, Yuho| Muraoka, Takayuki| Tanaka, Norimitsu| Shien, Kazuhiko| Furukawa, Masashi| Yamatsuji, Tomoki| Kiura, Katsuyuki| Naomoto, Yoshio| Miyoshi, Shinichiro|
Published Date 2012-04
Publication Title Lung Cancer
Volume volume76
Issue issue1
Content Type Journal Article
Author Kiura, Katsuyuki|
Published Date 2013-08-01
Publication Title 岡山医学会雑誌
Volume volume125
Issue issue2
Content Type Journal Article
Author Takeda, Hiromasa| Takigawa, Nagio| Ohashi, Kadoaki| Minami, Daisuke| Kataoka, Itaru| Ichihara, Eiki| Ochi, Nobuaki| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-02-15
Publication Title Experimental Cell Research
Volume volume319
Issue issue4
Content Type Journal Article
Author Ninomiya, Takashi| Takigawa, Nagio| Ichihara, Eiki| Ochi, Nobuaki| Murakami, Toshi| Honda, Yoshihiro| Kubo, Toshio| Minami, Daisuke| Kudo, Kenichiro| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-05
Publication Title Molecular Cancer Therapeutics
Volume volume12
Issue issue5
Content Type Journal Article
Title Alternative Treatment for a non-compliant patient with cancer and epilepsy
FullText URL 126_133.pdf
Author Minami, Daisuke| Ichihara, Eiki| Okabe, Nobuyuki| Yokomichi, Naosuke| Kouge, Noriko| Kajizono, Makoto| Akimoto, Yutaka| Hori, Keisuke| Matsubara, Minoru| Nasu, Junichiro| Tanimoto, Mitsune| Kiura, Katsuyuki| Matsuoka, Junzi|
Abstract  A 58-year-old man with cervical esophageal cancer and a history of epilepsy was treated with chemoradiotherapy from May of 2013. When tube feeding was initiated due to aspiration pneumonitis, the patient showed a degree of irritability that affected routine staff work and treatment compliance. We attempted to perform supportive care for maladjustment by the notice, the fast, and the tube feeding, but there was no improvement. After we added carbamazepine, primidone, and propericiazine (which had been canceled at the initiation of the tube feeding) to the patient's intravenous phenytoin, the symptoms and treatment compliance improved significantly. We concluded that the causes of the patient's irritability were maladjustment and his epilepsy.
Keywords てんかん(epilepsy) 易怒性(irritability) 適応障害(maladjustment)
Publication Title 岡山医学会雑誌
Published Date 2014-08-01
Volume volume126
Issue issue2
Start Page 133
End Page 135
ISSN 0030-1558
language 日本語
Copyright Holders Copyright (c) 2014 岡山医学会
File Version publisher
DOI 10.4044/joma.126.133
NAID 130004685264