著者 Takeda, Hiromasa| Takigawa, Nagio| Ohashi, Kadoaki| Minami, Daisuke| Kataoka, Itaru| Ichihara, Eiki| Ochi, Nobuaki| Tanimoto, Mitsune| Kiura, Katsuyuki|
発行日 2013-02-15
出版物タイトル Experimental Cell Research
319巻
4号
資料タイプ 学術雑誌論文
著者 木浦 勝行|
発行日 2013-08-01
出版物タイトル 岡山医学会雑誌
125巻
2号
資料タイプ 学術雑誌論文
著者 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|
発行日 2012-04
出版物タイトル Lung Cancer
76巻
1号
資料タイプ 学術雑誌論文
著者 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|
発行日 2012-07
出版物タイトル Lung Cancer
77巻
1号
資料タイプ 学術雑誌論文
著者 Harada, Daijiro| Takigawa, Nagio| Ochi, Nobuaki| Ninomiya, Takashi| Yasugi, Masayuki| Kubo, Toshio| Takeda, Hiromasa| Ichihara, Eiki| Ohashi, Kadoaki| Takata, Saburo| Tanimoto, Mitsune| Kiura, Katsuyuki|
発行日 2012-10
出版物タイトル Cancer Science
103巻
10号
資料タイプ 学術雑誌論文
著者 Kubo, Toshio| Takigawa, Nagio| Osawa, Masahiro| Harada, Daijiro| Ninomiya, Takashi| Ochi, Nobuaki| Ichihara, Eiki| Yamane, Hiromichi| Tanimoto, Mitsune| Kiura, Katsuyuki|
発行日 2013-01
出版物タイトル Cancer Science
104巻
1号
資料タイプ 学術雑誌論文
著者 Rai, Kammei| Takigawa, Nagio| Ito, Sachio| Kashihara, Hiromi| Ichihara, Eiki| Yasuda, Tatsuji| Shimizu, Kenji| Tanimoto, Mitsune| Kiura, Katsuyuki|
発行日 2011-09
出版物タイトル Molecular Cancer Therapeutics
10巻
9号
資料タイプ 学術雑誌論文
著者 木浦 勝行| 谷本 光音|
発行日 2013-04-01
出版物タイトル 岡山医学会雑誌
125巻
1号
資料タイプ 学術雑誌論文
著者 頼 冠名| 瀧川 奈義夫| 伊藤 佐智夫| 柏原 宏美| 市原 英基| 保田 立二| 清水 憲二| 谷本 光音| 木浦 勝行|
発行日 2012-12-03
出版物タイトル 岡山医学会雑誌
124巻
3号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/48564
フルテキストURL 66_3_245.pdf
著者 Okada, Toshiaki| Takigawa, Nagio| Kishino, Daizo| Katayama, Hideki| Kuyama, Shouichi| Sato, Ken| Mimoto, Junko| Ueoka, Hiroshi| Tanimoto, Mitsune| Kiura, Katsuyuki|
抄録 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).
キーワード cisplatin non-small cell lung cancer celecoxib cyclooxygenase-2 chemoprevention
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2012-06
66巻
3号
出版者 Okayama University Medical School
開始ページ 245
終了ページ 251
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2012 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 22729105
Web of Science KeyUT 000305669700008
JaLCDOI 10.18926/AMO/47260
フルテキストURL 65_6_353.pdf
著者 Ichihara, Eiki| Kiura, Katsuyuki| Tanimoto, Mitsune|
抄録 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.
キーワード angiogenesis cancer
Amo Type Review
出版物タイトル Acta Medica Okayama
発行日 2011-12
65巻
6号
出版者 Okayama University Medical School
開始ページ 353
終了ページ 362
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 22189475
Web of Science KeyUT 000298516900001
著者 谷口 暁| 宮原 信明| 中原 淳| 高田 三郎| 佐久川 亮| 長野 修| 谷本 安| 金廣 有彦| 木浦 勝行| 氏家 良人| 谷本 光音|
発行日 2011-12-01
出版物タイトル 岡山医学会雑誌
123巻
3号
資料タイプ 学術雑誌論文
著者 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|
発行日 2011-10
出版物タイトル Lung Cancer
74巻
1号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/46851
フルテキストURL 65_4_259.pdf
著者 Ogata, Yoshiko| Aoe, Keisuke| Hiraki, Akio| Murakami, Kazuo| Kishino, Daizo| Chikamori, Kenichi| Maeda, Tadashi| Ueoka, Hiroshi| Kiura, Katsuyuki| Tanimoto, Mitsune|
抄録 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.
キーワード pleural effusion adenosine deaminase tuberculosis lung cancer mesothelioma
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2011-08
65巻
4号
出版者 Okayama University Medical School
開始ページ 259
終了ページ 263
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 21860532
Web of Science KeyUT 000294236700006
著者 市原 英基| 大橋 圭明| 瀧川 奈義夫| 大澤 昌宏| 荻野 敦子| 谷本 光音| 木浦 勝行|
発行日 2011-04-01
出版物タイトル 岡山医学会雑誌
123巻
1号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/40503
フルテキストURL 64_5_285.pdf
著者 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|
抄録 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.
キーワード cancer of unknown primary site (CUP) cisplatin docetaxel prognosis
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2010-10
64巻
5号
出版者 Okayama University Medical School
開始ページ 285
終了ページ 291
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2010 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 20975761
Web of Science KeyUT 000283563300003
JaLCDOI 10.18926/AMO/32866
フルテキストURL fulltext.pdf
著者 Fujimoto, Nobukazu| Kiura, Katsuyuki| Takigawa, Nagio| Fujiwara, Yoshiro| Toyooka, Shinichi| Umemura, Shigeki| Tabata, Masahiro| Ueoka, Hiroshi| Tanimoto, Mitsune|
抄録 <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>
キーワード cisplatin docetaxel irinotecan triplet chemotherapy gefitinib
Amo Type Original Article
出版物タイトル Acta Medica Okayama
発行日 2010-02
64巻
1号
出版者 Okayama University Medical School
開始ページ 33
終了ページ 37
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 20200582
Web of Science KeyUT 000274868300005
JaLCDOI 10.18926/AMO/32669
フルテキストURL fulltext.pdf
著者 Takigawa, Nagio| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro|
抄録 <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>
キーワード small cell lung cancer etoposide-resistant cell line P-glycoprotein topoisomerase
Amo Type Article
出版物タイトル Acta Medica Okayama
発行日 1992-06
46巻
3号
出版者 Okayama University Medical School
開始ページ 203
終了ページ 212
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 1354408
Web of Science KeyUT A1992JB50400009
JaLCDOI 10.18926/AMO/32631
フルテキストURL fulltext.pdf
著者 Takigawa, Nagio| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro|
抄録 <p>In an attempt to predict the clinical activity of newly developed anthracycline analogues, ME2303, KRN8602, and SM5887 in the treatment of lung cancer, we compared antitumor activity of these drugs with that of adriamycin, using six human lung cancer cell lines and two drug-resistant human lung cancer sublines. Taking the pharmacokinetic data into consideration, we evaluated the relative antitumor activity: the ratio of area under the concentration-time curve of each drug to the 50% inhibitory concentration of the drug. Regarding this ratio, ME2303 was more potent than adriamycin, SM5887, and KRN8602. Cross-resistance of the new analogues to adriamycin was investigated using an adriamycin-resistant small cell lung cancer subline, SBC-3/ADM100 and an etoposide-resistant subline, SBC-3/ETP. SBC-3/ADM100 being 106-fold more resistant to adriamycin than the parent SBC-3 showed less resistance to the analogues: 1.80-fold to KRN8602, 3.80-fold to SM5887, and 8.60-fold to ME2303. SBC-3/ETP which was 52.1-fold more resistant to etoposide and 39.5-fold more resistant to adriamycin were also less resistant to the new analogues: 3.27-fold to KRN8602, 9.07-fold to SM5887, and 17.3-fold to ME2303. In conclusion, ME2303 was found to be the most potent agent among drugs tested for the treatment of lung cancer, and KRN8602 can be expected to be beneficial for the treatment of drug-resistant small cell lung cancer.</p>
キーワード new anthracycline analogues ME2303 KRN8602 SM5887 lung cancer cell line
Amo Type Article
出版物タイトル Acta Medica Okayama
発行日 1992-08
46巻
4号
出版者 Okayama University Medical School
開始ページ 249
終了ページ 256
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 1442149
Web of Science KeyUT A1992JL44200004
JaLCDOI 10.18926/AMO/32200
フルテキストURL fulltext.pdf
著者 Ohnoshi, Taisuke| Hiraki, Shunkichi| Ueda, Nobuo| Fujii, Masafumi| Machida, Ken-ichi| Ueoka, Hiroshi| Kawahara, Shin| Kozuka, Akira| Kiura, Katsuyuki| Moritaka, Tomonori| Kodani, Tsuyoshi| Kamei, Haruhito| Kimura, Ikuro|
抄録 <p>Twenty-seven previously untreated patients with unresectable non-small cell lung cancer were treated with a 3-drug combination of ifosfamide, cisplatin, and vindesine as a phase II study. Patients received ifosfamide, 1.3g/m2, on days 1 to 5; cisplatin, 20mg/m2, on days 1 to 5; and vindesine, 3mg/m2, on days 1 and 8; with a sufficient parenteral hydration. Courses were repeated every 4 weeks. Twenty males and seven females with a median age of 61 years were treated and fully evaluated. Five patients had stage IIIA, seven had stage IIIB, and 15 had stage IV disease. One patient with adenocarcinoma achieved a complete response and 16 achieved a partial response, for an overall response rate of 63% (95% confidence limit: 45% to 81%). The median duration of response was 34 weeks (range: 9 to 52 weeks). The median survival time was 58 weeks for patients with IIIA/B disease, and 33 weeks for those with IV disease. The major toxicity was myelosuppression, however, it was generally well-tolerated. These results indicate that the 3-drug combination is active against non-small cell lung cancer and warrants further clinical trials.</p>
キーワード non-small cell lung cancer ifosfamide cisplatin vindesine
Amo Type Article
出版物タイトル Acta Medica Okayama
発行日 1991-10
45巻
5号
出版者 Okayama University Medical School
開始ページ 357
終了ページ 361
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 1661559
Web of Science KeyUT A1991GN53800010