Author Gotoda, Tatsuhiro| Kawano, Seiji| Kono, Yoshiyasu| Miura, Kou| Kanzaki, Hiromitsu| Iwamuro, Masaya| Kawahara, Yoshiro| Tanaka, Takehiro| Yoshino, Tadashi| Shirakawad, Yasuhiro| Tabata, Masahiro| Tanimoto, Mitsune| Okada, Hiroyuki|
Published Date 2016-12-01
Publication Title Journal of Okayama Medical Association
Volume volume128
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/54607
FullText URL 70_5_425.pdf
Author Tamura, Tomoki| Hirata, Taizo| Tabata, Masahiro| Hinotsu, Shiro| Hamada, Akinobu| Motoki, Takayuki| Iwamoto, Takayuki| Mizoo, Taeko| Nogami, Tomohiro| Shien, Tadahiko| Taira, Naruto| Matsuoka, Junji| Doihara, Hiroyoshi|
Abstract Docetaxel is a standard treatment for patients with advanced or recurrent breast cancer. The recommended dose is 60 to 100 mg/m2. Previous study have shown that the tumor response rates of patients who received docetaxel monotherapy at doses of 60, 75, and 100 mg/m2 were 22.1% , 23.3% , and 36.0% , respectively, and there was a significant relationship between the dose and response. In Europe and the United States, docetaxel is approved at a dose of 100 mg/m2, and Japanese guidelines also recommend a dose of 100 mg/m2. However, the approved dose in Japan is up to 75 mg/m2. We have launched a phase I trial evaluating 100 mg/m2 docetaxel in patients with advanced or relapsed breast cancer. The major eligibility criteria are as follows: age ≥20 years, pathologically diagnosed breast cancer, recurrent or advanced breast cancer, a good performance status, and HER2 [human epidermal growth factor receptor 2] negative. The primary endpoint is demonstrated safety of 100 mg/m2 docetaxel. This study will clarify whether 100mg/m2 docetaxel can be administrated safely in Japanese patients with advanced or recurrent breast cancer.
Keywords breast cancer phase I trial docetaxel
Amo Type Clinical Study Protocols
Published Date 2016-10
Publication Title Acta Medica Okayama
Volume volume70
Issue issue5
Publisher Okayama University Medical School
Start Page 425
End Page 427
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 27777441
Web of Sience KeyUT 000388098700018
Sort Key 9
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
Note 特集(Feature Articles)
Publication Title 岡山医学会雑誌
Published Date 2015-08-03
Volume volume127
Issue issue2
Publisher 岡山医学会
Publisher Alternative Okayama Medical Association
Start Page 127
End Page 132
ISSN 0030-1558
NCID AN00032489
Content Type Journal Article
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
Refereed True
DOI 10.4044/joma.127.127
NAID 130005096256
Eprints Journal Name joma
References 1) Ohnoshi T, Hiraki S, Kawahara S, Yamashita H, Yonei T, Ishii J, Egawa T, Kozuka A, Hiraki Y, Kimura I : Randomized trial comparing chemotherapy alone and chemotherapy plus chest irradiation in limited stage small cell lung cancer : a preliminary report. Jpn J Clin Oncol (1986) 16, 271-277. 2) Pignon JP, Arriagada R, Ihde DC, Johnson DH, Perry MC, Souhami RL, Brodin O, Joss RA, Kies MS, Lebeau B, Onoshi T, Østerlind K, et al. : A meta-analysis of thoracic radiotherapy for small-cell lung cancer. N Engl J Med (1992) 327, 1618-1624. 3) Hotta K, Matsuo K, Ueoka H, Kiura K, Tabata M, Tanimoto M : Meta-analysis of randomized clinical trials comparing Cisplatin to Carboplatin in patients with advanced non-small-cell lung cancer. J Clin Oncol (2004) 22, 3852-3859. 4) Segawa Y, Kiura K, Takigawa N, Kamei H, Harita S, Hiraki S, Watanabe Y, Sugimoto K, Shibayama T, Yonei T, Ueoka H, Takemoto M, et al. : Phase III trial comparing docetaxel and cisplatin combination chemotherapy with mitomycin, vindesine, and cisplatin combination chemotherapy with concurrent thoracic radiotherapy in locally advanced non-small-cell lung cancer : OLCSG 0007. J Clin Oncol (2010) 28, 3299-3306. 5) EBMの手法による肺癌診療ガイドライン2014年版, 日本肺癌学会編, 金原出版, 東京 (2014) . 6) Kuyama S, Hotta K, Tabata M, Segawa Y, Fujiwara Y, Takigawa N, Kiura K, Ueoka H, Eguchi K, Tanimoto M : Impact of HER2 gene and protein status on the treatment outcome of cisplatin-based chemoradiotherapy for locally advanced non-small cell lung cancer. J Thorac Oncol (2008) 3, 477-482. 7) Mazières J, Peters S, Lepage B, Cortot AB, Barlesi F, Beau-Faller M, Besse B, Blons H, Mansuet-Lupo A, Urban T, Moro-Sibilot D, Dansin E, et al. : Lung cancer that harbors an HER2 mutation : epidemiologic characteristics and therapeutic perspectives. J Clin Oncol (2013) 31, 1997-2003. 8) Suzuki M, Shiraishi K, Yoshida A, Shimada Y, Suzuki K, Asamura H, Furuta K, Kohno T, Tsuta K : HER2 gene mutations in non-small cell lung carcinomas : Concurrence with her2 gene amplification and her2 protein expression and phosphorylation. Lung Cancer (2015) 87, 14-22. 9) Remillard S, Rebhun LI, Howie GA, Kupchan SM : Antimitotic activity of the potent tumor inhibitor maytansine. Science (1975) 189, 1002-1005. 10) Lewis Phillips GD, Li G, Dugger DL, Crocker LM, Parsons KL, Mai E, Blättler WA, Lambert JM, Chari RV, Lutz RJ, Wong WL, Jacobson FS, et al. : Targeting HER2-positive breast cancer with trastuzumab-DM1, an antibody-cytotoxic drug conjugate. Cancer Res (2008) 68, 9280-9290. 11) Weiler D, Diebold J, Strobel K, Aebi S, Gautschi O : Rapid response to trastuzumab emtansine in a patient with HER2-driven lung cancer. J Thorac Oncol (2015) 10, e16-17.
Author Ochi, Nobuaki| Takigawa, Nagio| Harada, Daijiro| Yasugi, Masayuki| Ichihara, Eiki| Hotta, Katsuyuki| Tabata, Masahiro| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2014-03-10
Publication Title Experimental Cell Research
Volume volume322
Issue issue1
Content Type Journal Article
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
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 Sience KeyUT 000274868300005
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 Sience KeyUT 000176521200002
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 Sience KeyUT 000178668100007
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 Sience KeyUT 000080058700002
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 Sience KeyUT A1993LL12400008
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/6296
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 Sience KeyUT A1993LL12400007
JaLCDOI 10.18926/AMO/31553
FullText URL fulltext.pdf
Author Tabata, Masahiro| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro|
Abstract <p>We report a preliminary study to determine whether MDR1 gene expression level in small cell lung cancer (SCLC) tumors is a useful predictor of tumor response to chemotherapy and patient survival in association with myc amplification in the tumor. We analyzed 18 patients with SCLC receiving adriamycin and etoposide combination chemotherapy between August 1989 and November 1991; 16 males and 2 females, median age of 68 years, and 7 with limited disease and 11 with extensive disease. MDR1 mRNA expression level and myc family gene amplification were simultaneously determined by polymerase chain reaction using transbronchial biopsy specimens which were obtained at diagnosis. Patients with tumors expressing low MDR1 mRNA responded more favorably to chemotherapy than those with tumors expressing high MDRI mRNA, however, the difference in tumor response was statistically not significant (84.6% versus 40%). The overall survival was significantly shorter in the latter than in the former (7.2 months versus 11.7 months; p = 0.023). The survival of the 4 patients with tumor showing myc family gene amplification was almost identical to that of patients with tumors showing no amplification of the gene (8.2 months versus 8.8 months; p = 0.73). Multivariate Cox's regression analysis supports the notion that MDR1 may be a useful independent prognostic factor.</p>
Keywords small cell lung cancer MDR1 mRNA expression myc gene amplification prognostic factor
Amo Type Article
Published Date 1993-08
Publication Title Acta Medica Okayama
Volume volume47
Issue issue4
Publisher Okayama University Medical School
Start Page 243
End Page 248
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 8213218
Web of Sience KeyUT A1993LV73800004
JaLCDOI 10.18926/AMO/31552
FullText URL fulltext.pdf
Author Yonei, Toshiro| Ohnoshi, Taisuke| Hiraki, Shunkichi| Ueoka, Hiroshi| Kiura, Katsuyuki| Moritaka, Tomonori| Shibayama, Takuo| Tabata, Masahiro| Segawa, Yoshihiko| Takigawa, Nagio| Kimura, Ikuro|
Abstract <p>Antitumor activities of five platinum analogs, including cisplatin, carboplatin, 254-S, DWA2114R, and NK121, were compared using five human lung cancer cell lines and 19 tumor specimens obtained from lung cancer patients. The antitumor activity was evaluated by determining the ratio of the maximum tolerated dose of each drug to the 70% tumor growth inhibitory concentration in a colony assay. Cisplatin was the most potent agent, followed by 254-S and carboplatin. DWA2114R and NK121 were less potent than cisplatin and 254-S. Cross-resistance to adriamycin was also investigated using an adriamycin-resistant small cell lung cancer subline, SBC -3/ADM30. SBC-3/ADM30 was 1.7- to 4.0-fold more resistant to cisplatin, carboplatin, NK121, and DWA2114R, than was the parent line, SBC-3, and the subline was 2.0-fold more sensitive to 254-S. Using SBC-3, in vitro combination effects of etoposide and cisplatin, carboplatin, or 254-S were evaluated by the median-effect principle. Synergism was noted when cisplatin and etoposide were combined at a fixed molar ratio of 1:1. Combination of carboplatin and etoposide showed an additive effect. The combination of 254-S and etoposide was antagonistic at low concentrations, but was markedly synergistic at higher concentrations. These data suggested the efficacy of 254-S in the treatment of lung cancer.</p>
Keywords platinum analogs antitumor activity lung cancer colony assay combination effect
Amo Type Article
Published Date 1993-08
Publication Title Acta Medica Okayama
Volume volume47
Issue issue4
Publisher Okayama University Medical School
Start Page 233
End Page 241
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 8213217
Web of Sience KeyUT A1993LV73800003
JaLCDOI 10.18926/AMO/31310
FullText URL fulltext.pdf
Author Tamura, Makoto| Ueoka, Hiroshi| Kiura, Katsuyuki| Tabata, Masahiro| Shibayama, Takuo| Miyatake, Kazuyo| Genba, Kenichi| Hiraki, Shunkichi| harada, Mine|
Abstract <p>In order to elucidate factors influencing the prognosis of small-cell lung cancer (SCLC), we reviewed the records of 253 patients with SCLC and evaluated 20 pretreatment prognostic factors by univariate analysis and Cox's multiple regression analysis. Recursive partitioning and amalgamation (RPA) was employed to identify subgroups with similar survival rates. Cox's multiple regression analysis identified five significant factors: extent of disease, number of metastatic sites, serum albumin, serum lactate dehydrogenase, and presence of weight loss. Among these, extent of disease was the most influential factor. RPA analysis revealed three subgroups predicting significantly different prognoses. The median survival time and 3-year survival rate were 18.4 months and 20.6%, respectively for the good-risk group (limited disease without weight loss), 13.5 months and 9.1%, respectively for the intermediate-risk group (limited disease with weight loss or extensive disease with less than two metastatic sites), and 9.2 months and 0%, respectively for the poor-risk group (extensive disease with two or more metastatic sites). These results will be useful for development of new staging system or subsequent stratification for randomized trials.</p>
Keywords prognostic factors Cox's multiple regression analysis recursive partitioning and amalgamayion method small-sell lung canser
Amo Type Article
Published Date 1998-04
Publication Title Acta Medica Okayama
Volume volume52
Issue issue2
Publisher Okayama University Medical School
Start Page 105
End Page 111
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 9588226
Web of Sience KeyUT 000073363000006
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 Sience KeyUT A1997XJ12700002
JaLCDOI 10.18926/AMO/30751
FullText URL fulltext.pdf
Author Kitajima, Takuji| Nishii, Kenji| Ueoka, Hiroshi| Shibayama, Takuo| Gemba, Kenichi| Kodani, Tsuyoshi| Kiura, Katsuyuki| Tabata, Masahiro| Hotta, Katsuyuki| Tanimoto, Mitsune| Sobue, Tomotaka|
Abstract <p>To evaluate recent improvements in lung cancer screening, we compared the results of recently conducted lung cancer screening with those of a previous screening. This study compared the survival of lung cancer patients detected by lung cancer screening conducted between 1976 and 1984 (early period) with that conducted between 1989 and 1997 (late period). Two hundred seventy-six patients with lung cancer were detected in the early period and 541 patients with lung cancer were detected in the late period. The median survival time (late : 49.8 vs. early : 27.8 months) and the 5-year survival rate (late : 47.8 vs. early : 34.8%) of the patients with lung cancer detected in the late period were significantly better than those in the early period (p = 0.0054). Among patients undergoing resection, the proportion of pathological stage I patients in the late period was significantly higher than that in the early period (late : 60.8 vs. early : 54.9%, p = 0.005). Multivariate analysis showed that the screening time period was a significant prognostic factor (hazard ratio = 0.685, 95% confidence interval : 0.563-0.832, p = 0.0002). These results were consistent with the findings of case-control studies of lung cancer screening programs in the late period recently conducted in Japan, which also showed a greater efficacy for screening than for previous case-control studies in the early period.</p>
Keywords lung cancer screening survival lung cancer mortality
Amo Type Article
Published Date 2006-06
Publication Title Acta Medica Okayama
Volume volume60
Issue issue3
Publisher Okayama University Medical School
Start Page 173
End Page 179
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 16838046
Web of Sience KeyUT 000238503600005
JaLCDOI 10.18926/AMO/30737
FullText URL fulltext.pdf
Author Suzaki, Noriyuki| Hiraki, Akio| Takigawa, Nagio| Ueoka, Hiroshi| Tanimoto, Yasushi| Kozuki, Toshiyuki| Tabata, Masahiro| Kanehiro, Arihiko| Kiura, Katsuyuki| Tanimoto, Mitsune|
Abstract A 71-year-old Japanese man with adenocarcinoma of the lung developed interstitial pneumonia after treatment with paclitaxel. The patient had acute chills and fever on the fourth day after the second exposure to paclitaxel, rapidly got worse despite empiric therapies, and developed prolonged respiratory failure requiring mechanical ventilation. Four months later, he died of respiratory failure due to progression of both interstitial pneumonia and lung cancer. This is the first case developing fatal paclitaxel-induced pulmonary toxicity to date. Interstitial pneumonia should be considered one of the possible life-threatening complications during treatment with paclitaxel.
Keywords paclitaxel adverse effect lung cancer interstitial pneumonia
Amo Type Article
Published Date 2006-10
Publication Title Acta Medica Okayama
Volume volume60
Issue issue5
Publisher Okayama University Medical School
Start Page 295
End Page 298
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 17072376
Web of Sience KeyUT 000241509000006
Author Matsuoka, Junji| Naomoto, Yoshio| Tabata, Masahiro| Shirakawa, Yasuhiro| Hotta, Katsuyuki| Tanimoto, Mitsune| Tanaka, Noriaki|
Published Date 2009-04-01
Publication Title 岡山医学会雑誌
Volume volume121
Issue issue1
Content Type Journal Article
Author 木浦 勝行| 谷本 安| 田端 雅弘| 金廣 有彦| 上岡 博| 谷本 光音| 渡邊 都貴子| 草野 展周| 小出 典男|
Published Date 2005-05-30
Publication Title 岡山医学会雑誌
Volume volume115
Issue issue1
Content Type Journal Article
Author Gochi, Akira| Senami, Hisako| Ohara, Naomi| Tabata, Masahiro|
Published Date 2007-05-01
Publication Title 岡山医学会雑誌
Volume volume119
Issue issue1
Content Type Journal Article