Author | Kiura, Katsuyuki| |
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Published Date | 1993-09-30 |
Publication Title | |
Content Type | Thesis or Dissertation |
Author | Kiura, Katsuyuki| Takigawa, Nagio| Oze, Isao| Yasugi, Masayuki| Ochi, Nobuaki| Harada, Daijiro| Tanimoto, Mitsune| |
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Published Date | 2008-01-04 |
Publication Title | 岡山医学会雑誌 |
Volume | volume119 |
Issue | issue3 |
Content Type | Journal Article |
Author | 谷本 安| 佐久川 亮| 木浦 勝行| 谷本 光音| |
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Published Date | 2005-01-31 |
Publication Title | 岡山医学会雑誌 |
Volume | volume116 |
Issue | issue3 |
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| |
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Published Date | 2005-05-30 |
Publication Title | 岡山医学会雑誌 |
Volume | volume115 |
Issue | issue1 |
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| |
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Published Date | 2008-12-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume120 |
Issue | issue3 |
Content Type | Journal Article |
Author | Ichihara, Eiki| Matsuoka, Junji| Takigawa, Nagio| Matsuzaki, Takashi| Katsui, Kuniaki| Kiura, Katsuyuki| Tanimoto, Mitsune| |
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Published Date | 2009-12-01 |
Publication Title | 岡山医学会雑誌 |
Volume | volume121 |
Issue | issue3 |
Content Type | Journal Article |
JaLCDOI | 10.18926/AMO/30737 |
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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 |
Publication Title | Acta Medica Okayama |
Published Date | 2006-10 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 17072376 |
Web of Science KeyUT | 000241509000006 |
JaLCDOI | 10.18926/AMO/30751 |
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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 | 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. |
Keywords | lung cancer screening survival lung cancer mortality |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 2006-06 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 16838046 |
Web of Science KeyUT | 000238503600005 |
JaLCDOI | 10.18926/AMO/30795 |
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FullText URL | fulltext.pdf |
Author | Matsuo, Keisuke| Kiura, Katsuyuki| Ueoka, Hiroshi| Tabata, Masahiro| Shibayama, Takuo| Matsumura, Tadashi| Takigawa, Nagio| Hiraki, Shunkichi| Harada, Mine| |
Abstract | 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. |
Keywords | Adriamycin-resistant cell line antifolates small cell lung cancer |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1997-06 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 9227790 |
Web of Science KeyUT | A1997XJ12700002 |
JaLCDOI | 10.18926/AMO/31310 |
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FullText URL | fulltext.pdf |
Author | Tamura, Makoto| Ueoka, Hiroshi| Kiura, Katsuyuki| Tabata, Masahiro| Shibayama, Takuo| Miyatake, Kazuyo| Genba, Kenichi| Hiraki, Shunkichi| harada, Mine| |
Abstract | 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. |
Keywords | prognostic factors Cox's multiple regression analysis recursive partitioning and amalgamayion method small-sell lung canser |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1998-04 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 9588226 |
Web of Science KeyUT | 000073363000006 |
JaLCDOI | 10.18926/AMO/31552 |
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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 | 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. |
Keywords | platinum analogs antitumor activity lung cancer colony assay combination effect |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1993-08 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 8213217 |
Web of Science KeyUT | A1993LV73800003 |
JaLCDOI | 10.18926/AMO/31553 |
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FullText URL | fulltext.pdf |
Author | Tabata, Masahiro| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro| |
Abstract | 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. |
Keywords | small cell lung cancer MDR1 mRNA expression myc gene amplification prognostic factor |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1993-08 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 8213218 |
Web of Science KeyUT | A1993LV73800004 |
JaLCDOI | 10.18926/AMO/31590 |
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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 | 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. |
Keywords | small cell lung cancer immunohistochemistry drug resistance P-glycoprotein carcinoembryonic antigen |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1993-06 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 8104371 |
Web of Science KeyUT | A1993LL12400007 |
JaLCDOI | 10.18926/AMO/31591 |
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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 | 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. |
Keywords | small cell lung cancer long-term survivors late relapse toxicities complications |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1993-06 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 8397470 |
Web of Science KeyUT | A1993LL12400010 |
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 |
Publication Title | Acta Medica Okayama |
Published Date | 1993-06 |
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 | English |
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 |
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 | 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. |
Keywords | drug screening system MTT assay lung cancer cell line drug resistance |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1999-04 |
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 | English |
File Version | publisher |
Refereed | True |
Web of Science KeyUT | 000080058700002 |
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 | 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. |
Keywords | non-small-cell lung cancer concurrent chemoradiotherapy low-dose cisplatin poor-risk factor |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 2002-10 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 12530510 |
Web of Science KeyUT | 000178668100007 |
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 | 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. |
Keywords | chemosensitivity test 3-(4 5-dimethylthiazol-2-yl)-2 5-diphenyltertrazolium bromide (MTT) assay clonogenic assay |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 2002-06 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 12108583 |
Web of Science KeyUT | 000176521200002 |
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 | 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. |
Keywords | non-small cell lung cancer ifosfamide cisplatin vindesine |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1991-10 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 1661559 |
Web of Science KeyUT | A1991GN53800010 |
JaLCDOI | 10.18926/AMO/32631 |
---|---|
FullText URL | fulltext.pdf |
Author | Takigawa, Nagio| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro| |
Abstract | 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. |
Keywords | new anthracycline analogues ME2303 KRN8602 SM5887 lung cancer cell line |
Amo Type | Article |
Publication Title | Acta Medica Okayama |
Published Date | 1992-08 |
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 | English |
File Version | publisher |
Refereed | True |
PubMed ID | 1442149 |
Web of Science KeyUT | A1992JL44200004 |