| 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 | 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 | 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 |
| 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 |
| 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/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 | 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/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 |
| 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/32631 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Takigawa, Nagio| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro| |
| Abstract | <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> |
| Keywords | new anthracycline analogues ME2303 KRN8602 SM5887 lung cancer cell line |
| Amo Type | Article |
| Published Date | 1992-08 |
| Publication Title | Acta Medica Okayama |
| Volume | volume46 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 249 |
| End Page | 256 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 1442149 |
| Web of Science KeyUT | A1992JL44200004 |
| JaLCDOI | 10.18926/AMO/32200 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | 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| |
| Abstract | <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> |
| Keywords | non-small cell lung cancer ifosfamide cisplatin vindesine |
| Amo Type | Article |
| Published Date | 1991-10 |
| Publication Title | Acta Medica Okayama |
| Volume | volume45 |
| Issue | issue5 |
| Publisher | Okayama University Medical School |
| Start Page | 357 |
| End Page | 361 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 1661559 |
| Web of Science KeyUT | A1991GN53800010 |
| JaLCDOI | 10.18926/AMO/31591 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Ohnoshi, Taisuke| Hiraki, Shunkichi| Fujii, Masafumi| Ueoka, Hiroshi| Yonei, Toshiro| Tamura, Makoto| Moritaka, Tomonori| Mima, Yuchi| Horiguchi, Takashi| Kiura, Katsuyuki| Kamei, Haruhito| Kodani, Tsuyoshi| Hiraki, Yoshio| Kimura, Ikuro| |
| Abstract | <p>We evaluated the long-term outcome of 148 patients with small cell lung cancer (SCLC) who had been entered into clinical trials of chemotherapy with or without thoracic and prophylactic cranial irradiation (PCI) between 1981 and 1987. Eighteen patients (12%) survived for 2 or more years. With a minimum follow-up of 4.5 years, 10 of the 18 patients who remained disease-free at 2 years are currently alive and free of SCLC. Seven of these 10 patients currently function as they did before diagnosis. However, three suffer from central nervous system changes of varying degrees in severity which appeared 2-3 years after PCI. Eight of the 18 patients who were disease-free at 2 years have died. Two died of isolated relapse in the brain at 3.6 and 4.2 years after initiation of chemotherapy. Five died of other malignancies while continuing their complete response to SCLC; two of non-small cell lung cancer, two of acute myelogenous leukemia, and one of hepatocellular carcinoma. Another patient died of an unrelated disease without any evidence of SCLC. A small but substantial proportion of patients who underwent intensive treatment will achieve long-term survival; however, these patients remain at higher risk for second cancers and late toxicities. Therefore, attention must be directed to defining the safest way to employ such treatment in the management of SCLC.</p> |
| Keywords | small cell lung cancer long-term survivors late relapse toxicities complications |
| Amo Type | Article |
| Published Date | 1993-06 |
| Publication Title | Acta Medica Okayama |
| Volume | volume47 |
| Issue | issue3 |
| Publisher | Okayama University Medical School |
| Start Page | 209 |
| End Page | 214 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 8397470 |
| Web of Science KeyUT | A1993LL12400010 |
| 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 |
| Author | Kiura, Katsuyuki| |
|---|---|
| Published Date | 1993-09-30 |
| Publication Title | |
| Content Type | Thesis or Dissertation |
