| JaLCDOI | 10.18926/AMO/54503 |
|---|---|
| FullText URL | 70_4_273.pdf |
| Author | Makimoto, Go| Miyahara, Nobuaki| Yoshikawa, Mao| Taniguchi, Akihiko| Kanehiro, Arihiko| Tanimoto, Mitsune| Kiura, Katsuyuki| |
| Abstract | Heerfordtʼs syndrome is a rare manifestation of sarcoidosis and is defined as a combination of facial palsy, parotid swelling, and uveitis, associated with a low-grade fever. We report a case of Heerfordtʼs syndrome presenting with a high fever and increased serum tumor necrosis factor alpha (TNF-α) levels. The patient had facial palsy, parotid swelling, uveitis, and swelling of the right supraclavicular and hilar lymph nodes. Corticosteroid therapy was initiated, and her symptoms soon resolved completely, in tandem with a decrease in TNF-α serum levels. |
| Keywords | Heerfordtʼs syndrome sarcoidosis TNF-α |
| Amo Type | Case Report |
| Published Date | 2016-08 |
| Publication Title | Acta Medica Okayama |
| Volume | volume70 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 273 |
| End Page | 277 |
| 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 | 27549672 |
| Web of Science KeyUT | 000384748600007 |
| 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 |
| Publication Title | 岡山医学会雑誌 |
| Published Date | 2015-08-03 |
| Volume | volume127 |
| Issue | issue2 |
| Start Page | 127 |
| End Page | 132 |
| ISSN | 0030-1558 |
| 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 |
| DOI | 10.4044/joma.127.127 |
| NAID | 130005096256 |
| 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 Science KeyUT | A1997XJ12700002 |
| Author | Yasugi, Masayuki| Takigawa, Nagio| Ochi, Nobuaki| Ohashi, Kadoaki| Harada, Daijiro| Ninomiya, Takashi| Murakami, Toshi| Honda, Yoshihiro| Ichihara, Eiki| Tanimoto, Mitsune| Kiura, Katsuyuki| |
|---|---|
| Published Date | 2014-08-15 |
| Publication Title | Experimental Cell Research |
| Volume | volume326 |
| Issue | issue2 |
| Content Type | Journal Article |
| 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 Science KeyUT | A1993LL12400008 |
| Related Url | http://ousar.lib.okayama-u.ac.jp/metadata/6296 |
| Author | Kiura, Katsuyuki| |
|---|---|
| Published Date | 1993-09-30 |
| Publication Title | |
| Content Type | Thesis or Dissertation |
| 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 Science KeyUT | 000080058700002 |
| 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/54499 |
|---|---|
| FullText URL | 70_4_243.pdf |
| Author | Osawa, Masahiro| Ohashi, Kadoaki| Kubo, Toshio| Ichihara, Eiki| Takata, Saburo| Takigawa, Nagio| Takata , Minoru| Tanimoto, Mitsune| Kiura, Katsuyuki| |
| Abstract | Vandetanib (ZactimaTM) is a novel, orally available inhibitor of both vascular endothelial growth factor receptor-2 (VEGFR-2) and epidermal growth factor receptor (EGFR) tyrosine kinase. In the present study, a line of transgenic mice with a mouse Egfr gene mutation (delE748-A752) corresponding to a human EGFR mutation (delE746-A750) was established. The transgenic mice developed atypical adenomatous hyperplasia to adenocarcinoma of the lung at around 5 weeks of age and died of lung tumors at approximately 17 weeks of age. In the mice treated with vandetanib (6mg/kg/day), these lung tumors disappeared and the phosphorylations of EGFR and VEGFR-2 were reduced in lung tissues to levels comparable to those of non-transgenic control mice. The median overall survival time of the transgenic mice was 28 weeks in the vandetanib-treated group and 17 weeks in the vehicle-treated group. Vandetanib significantly prolonged the survival of the transgenic mice (log-rank test, p＜0.01); resistance to vandetanib occurred at 20 weeks of age and the animals died from their lung tumors at about 28 weeks of age. These data suggest that vandetanib could suppress the progression of tumors harboring an activating EGFR mutation. |
| Keywords | vandetanib VEGFR EGFR nonsmall cell lung cancer transgenic mouse |
| Amo Type | Original Article |
| Published Date | 2016-08 |
| Publication Title | Acta Medica Okayama |
| Volume | volume70 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 243 |
| End Page | 253 |
| 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 | 27549668 |
| Web of Science KeyUT | 000384748600003 |
| Author | Murakami, Toshi| Takigawa, Nagio| Ninomiya, Takashi| Ochi, Nobuaki| Yasugi, Masaaki| Honda, Yoshihiro| Kubo, Toshio| Ichihara, Eiki| Hotta, Katsuyuki| Tanimoto, Mitsune| Kiura, Katsuyuki| |
|---|---|
| Published Date | 2014-01 |
| Publication Title | Lung Cancer |
| Volume | volume83 |
| Issue | issue1 |
| Content Type | Journal Article |
| Author | Rai, Kammei| Takigawa, Nagio| Ito, Sachio| Kashihara, Hiromi| Ichihara, Eiki| Yasuda, Tatsuji| Shimizu, Kenji| Tanimoto, Mitsune| Kiura, Katsuyuki| |
|---|---|
| Published Date | 2012-12-03 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume124 |
| Issue | issue3 |
| 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| |
|---|---|
| Published Date | 2008-12-01 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume120 |
| Issue | issue3 |
| Content Type | Journal Article |
| FullText URL | BMCC19_1_1144.pdf |
|---|---|
| Author | Katsui, Kuniaki| Ogata, Takeshi| Watanabe, Kenta| Katayama, Norihisa| Soh, Junichi| Kuroda, Masahiro| Kiura, Katsuyuki| Maeda, Yoshinobu| Toyooka, Shinichi| Kanazawa, Susumu| |
| Keywords | Induction chemoradiotherapy Lower lobe Mean lung dose Non-small cell lung cancer Radiation pneumonitis |
| Published Date | 2019-11 |
| Publication Title | BMC Cancer |
| Volume | volume19 |
| Issue | issue1 |
| Publisher | BMC |
| Start Page | 1144 |
| ISSN | 1471-2407 |
| Content Type | Journal Article |
| language | 英語 |
| OAI-PMH Set | 岡山大学 |
| Copyright Holders | © The Author(s). 2019 |
| File Version | publisher |
| PubMed ID | 31771538 |
| DOI | 10.1186/s12885-019-6359-9 |
| Web of Science KeyUT | 000499423900004 |
| Related Url | isVersionOf https://doi.org/10.1186/s12885-019-6359-9 |
| Author | Higo, Hisao| Miyahara, Nobuaki| Taniguchi, Akihiko| Senoo, Satoru| Itano, Junko| Watanabe, Hiromi| Oda, Naohiro| Kayatani, Hiroe| Ichikawa, Hirohisa| Shibayama, Takuo| Kajimoto, Kazuhiro| Tanimoto, Yasushi| Kanehiro, Arihiko| Maeda, Yoshinobu| Kiura, Katsuyuki| OKAYAMA respiratory disease study group (ORDSG)| |
|---|---|
| Keywords | Idiopathic pulmonary fibrosis High-resolution computed tomography Pirfenidone Forced vital capacity |
| Note | This fulltext is available in Feb. 2021.| |
| Published Date | 2020-02-23 |
| Publication Title | Respiratory Investigation |
| Volume | volume58 |
| Issue | issue3 |
| Publisher | Elsevier |
| Start Page | 185 |
| End Page | 189 |
| ISSN | 22125345 |
| NCID | AA12579673 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | author |
| PubMed ID | 32102769 |
| DOI | 10.1016/j.resinv.2019.12.007 |
| Web of Science KeyUT | 000531841500009 |
| Related Url | isVersionOf https://doi.org/10.1016/j.resinv.2019.12.007 |
| Author | Nishii, Kazuya| Ohashi, Kadoaki| Tamura, Tomoki| Ninomiya, Kiichiro| Matsubara, Takehiro| Senoo, Satoru| Kano, Hirohisa| Watanabe, Hiromi| Oda, Naohiro| Makimoto, Go| Higo, Hisao| Kato, Yuka| Ninomiya, Takashi| Kubo, Toshio| Yamamoto, Hiromasa | Tomida, Shuta| Hotta, Katsuyuki| Tabata, Masahiro| Toyooka, Shinichi| Maeda, Yoshinobu| Kiura, Katsuyuki| |
|---|---|
| Keywords | non-small cell lung cancer epidermal growth factor receptor mutations droplet digital PCR exhaled breath condensate EGFR-TKIs |
| Note | This fulltext is available in Apr. 2021.| |
| Published Date | 2020-12 |
| Publication Title | Oncology Letters |
| Volume | volume20 |
| Issue | issue6 |
| Publisher | Spandidos Publications |
| Start Page | 393 |
| ISSN | 1792-1074 |
| Content Type | Journal Article |
| language | 英語 |
| OAI-PMH Set | 岡山大学 |
| File Version | publisher |
| PubMed ID | 33193853 |
| DOI | 10.3892/ol.2020.12256 |
| Web of Science KeyUT | 000595649300005 |
| Related Url | isVersionOf https://doi.org/10.3892/ol.2020.12256 |
| 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 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 | <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 Science KeyUT | 000176521200002 |
| 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/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/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 Science KeyUT | A1993LV73800003 |
