フルテキストURL fulltext.pdf
著者 Itano, Junko| Ohashi, Kadoaki| Senoo, Satoru| Oda, Naohiro| Nishii, Kazuya| Taniguchi, Akihiko| Miyahara, Nobuaki| Maeda, Yoshinobu| Kiura, Katsuyuki|
キーワード Axillary lymphadenitis Mycobacterium avium complex infection Mycobacterium intracellulare
発行日 2019
出版物タイトル Respiratory Medicine Case Reports
28巻
出版者 Elsevier
開始ページ 100947
ISSN 2213-0071
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
著作権者 © 2019 The Authors.
論文のバージョン publisher
PubMed ID 31681532
DOI 10.1016/j.rmcr.2019.100947
Web of Science KeyUT 000511444900001
関連URL isVersionOf https://doi.org/10.1016/j.rmcr.2019.100947
著者 Nogami, Naoyuki| Hotta, Katsuyuki| Kuyama, Shoichi| Kiura, Katsuyuki| Takigawa, Nagio| Chikamori, Kenichi| Shibayama, Takuo| Kishino, Daizo| Hosokawa, Shinobu| Tamaoki, Akihiko| Harita, Shingo| Tabata, Masahiro| Ueoka, Hiroshi| Shinkai, Tetsu| Tanimoto, Mitsune|
発行日 2011-10
出版物タイトル Lung Cancer
74巻
1号
資料タイプ 学術雑誌論文
著者 Ninomiya, Takashi| Takigawa, Nagio| Ichihara, Eiki| Ochi, Nobuaki| Murakami, Toshi| Honda, Yoshihiro| Kubo, Toshio| Minami, Daisuke| Kudo, Kenichiro| Tanimoto, Mitsune| Kiura, Katsuyuki|
発行日 2013-05
出版物タイトル Molecular Cancer Therapeutics
12巻
5号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/60796
フルテキストURL 74_5_371.pdf
著者 Makimoto, Go| Ohashi, Kadoaki| Maeda, Yoshinobu| Kiura, Katsuyuki|
抄録 The prognosis of advanced non-small cell lung cancer (NSCLC) patients has improved in recent decades, especially for patients with an oncogenic driver mutation. Anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors (TKIs) are effective for patients with the echinoderm microtubule-associated protein-like 4-ALK fusion gene. Several ALK-TKIs have been established: the first-generation ALK-TKI, crizotinib; second-generation ALK-TKIs, alectinib and ceritinib; and third-generation ALK-TKI, lorlatinib. Some ALK-TKIs are effective for tumors that are resistant to other ALK-TKIs; however, as is known in epidermal growth factor receptormutant lung cancer, tumor resistance is inevitable. ALK-positive NSCLCs acquire resistance via various mechanisms, making it a heterogeneous disease. Therefore, it is necessary to develop next-generation treatment strategies, such as the use of next-generation ALK-TKIs for secondary mutations, or combination therapies with ALK-TKIs and other TKIs. In this review, we summarize the development and use of ALK-TKIs, prior pivotal clinical trials, and resistance mechanisms.
キーワード lung cancer anaplastic lymphoma kinase tyrosine kinase inhibitors resistance mechanism
Amo Type Review
発行日 2020-10
出版物タイトル Acta Medica Okayama
74巻
5号
出版者 Okayama University Medical School
開始ページ 371
終了ページ 379
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2020 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 33106692
JaLCDOI 10.18926/AMO/31552
フルテキストURL fulltext.pdf
著者 Yonei, Toshiro| Ohnoshi, Taisuke| Hiraki, Shunkichi| Ueoka, Hiroshi| Kiura, Katsuyuki| Moritaka, Tomonori| Shibayama, Takuo| Tabata, Masahiro| Segawa, Yoshihiko| Takigawa, Nagio| Kimura, Ikuro|
抄録 <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>
キーワード platinum analogs antitumor activity lung cancer colony assay combination effect
Amo Type Article
発行日 1993-08
出版物タイトル Acta Medica Okayama
47巻
4号
出版者 Okayama University Medical School
開始ページ 233
終了ページ 241
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 8213217
Web of Science KeyUT A1993LV73800003
JaLCDOI 10.18926/AMO/40503
フルテキストURL 64_5_285.pdf
著者 Nishimori, Hisakazu| Takahashi, Shunji| Kiura, Katsuyuki| Ennishi, Daisuke| Kobayashi, Takayuki| Sano, Koji| Shinozaki, Eiji| Yokoyama, Masahiro| Mishima, Yuko| Terui, Yasuhito| Chin, Keisho| Mizunuma, Nobuyuki| Ito, Yoshinori| Nishimura, Seiichiro| Takeuchi, Kengo| Ishikawa, Yuichi| Oguchi, Masahiko| Tanimoto, Mitsune| Hatake, Kiyohiko|
抄録 We evaluated the efficacy and toxicity of cisplatin/docetaxel (CDDP/TXT) chemotherapy and identified prognostic factors in Japanese patients with cancer of unknown primary site (CUP). Twenty-eight consecutive patients seen at a single institute were reviewed retrospectively. Sixteen patients were treated with TXT 80mg/m2, followed by CDDP 75mg/m2. The overall response rate to CDDP/TXT treatment was 62.5%, with a median survival time (MST) of 22.7 months. Common adverse reactions were myelosuppression and hyponatremia. The MST of all 28 patients with CUP was 8.3 months, and the 1-year overall survival rate was 45.6%. Univariate analysis identified 5 prognostic factors:performance status, liver involvement, bone involvement, pleural involvement, and lymph node involvement. In conclusion, CDDP/TXT chemotherapy is effective with tolerable toxicity in patients with CUP. Japanese patients with CUP might be chemosensitive and may survive longer.
キーワード cancer of unknown primary site (CUP) cisplatin docetaxel prognosis
Amo Type Original Article
発行日 2010-10
出版物タイトル Acta Medica Okayama
64巻
5号
出版者 Okayama University Medical School
開始ページ 285
終了ページ 291
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2010 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 20975761
Web of Science KeyUT 000283563300003
JaLCDOI 10.18926/AMO/32631
フルテキストURL fulltext.pdf
著者 Takigawa, Nagio| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro|
抄録 <p>In an attempt to predict the clinical activity of newly developed anthracycline analogues, ME2303, KRN8602, and SM5887 in the treatment of lung cancer, we compared antitumor activity of these drugs with that of adriamycin, using six human lung cancer cell lines and two drug-resistant human lung cancer sublines. Taking the pharmacokinetic data into consideration, we evaluated the relative antitumor activity: the ratio of area under the concentration-time curve of each drug to the 50% inhibitory concentration of the drug. Regarding this ratio, ME2303 was more potent than adriamycin, SM5887, and KRN8602. Cross-resistance of the new analogues to adriamycin was investigated using an adriamycin-resistant small cell lung cancer subline, SBC-3/ADM100 and an etoposide-resistant subline, SBC-3/ETP. SBC-3/ADM100 being 106-fold more resistant to adriamycin than the parent SBC-3 showed less resistance to the analogues: 1.80-fold to KRN8602, 3.80-fold to SM5887, and 8.60-fold to ME2303. SBC-3/ETP which was 52.1-fold more resistant to etoposide and 39.5-fold more resistant to adriamycin were also less resistant to the new analogues: 3.27-fold to KRN8602, 9.07-fold to SM5887, and 17.3-fold to ME2303. In conclusion, ME2303 was found to be the most potent agent among drugs tested for the treatment of lung cancer, and KRN8602 can be expected to be beneficial for the treatment of drug-resistant small cell lung cancer.</p>
キーワード new anthracycline analogues ME2303 KRN8602 SM5887 lung cancer cell line
Amo Type Article
発行日 1992-08
出版物タイトル Acta Medica Okayama
46巻
4号
出版者 Okayama University Medical School
開始ページ 249
終了ページ 256
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 1442149
Web of Science KeyUT A1992JL44200004
JaLCDOI 10.18926/AMO/31714
フルテキストURL fulltext.pdf
著者 Kawada, Kazuhiko| Yonei, Toshiro| Ueoka, Hiroshi| Kiura, Katsuyuki| Tabata, Masahiro| Takigawa, Nagio| Harada, Mine| Tanimoto, Mitsune|
抄録 <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>
キーワード chemosensitivity test 3-(4 5-dimethylthiazol-2-yl)-2 5-diphenyltertrazolium bromide (MTT) assay clonogenic assay
Amo Type Article
発行日 2002-06
出版物タイトル Acta Medica Okayama
56巻
3号
出版者 Okayama University Medical School
開始ページ 129
終了ページ 134
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 12108583
Web of Science KeyUT 000176521200002
JaLCDOI 10.18926/AMO/31705
フルテキストURL fulltext.pdf
著者 Takata, Ichiro| Ueoka, Hiroshi| Kiura, Katsuyuki| Tabata, Masahiro| Takigawa, Nagio| Katayama, Hideki| Takemoto, Mitsuhiro| Hiraki, Yoshio| Harada, Mine| Tanimoto, Mitsune|
抄録 <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>
キーワード non-small-cell lung cancer concurrent chemoradiotherapy low-dose cisplatin poor-risk factor
Amo Type Article
発行日 2002-10
出版物タイトル Acta Medica Okayama
56巻
5号
出版者 Okayama University Medical School
開始ページ 261
終了ページ 266
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 12530510
Web of Science KeyUT 000178668100007
著者 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|
キーワード non-small cell lung cancer epidermal growth factor receptor mutations droplet digital PCR exhaled breath condensate EGFR-TKIs
備考 This fulltext is available in Apr. 2021.|
発行日 2020-12
出版物タイトル Oncology Letters
20巻
6号
出版者 Spandidos Publications
開始ページ 393
ISSN 1792-1074
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
論文のバージョン publisher
PubMed ID 33193853
DOI 10.3892/ol.2020.12256
Web of Science KeyUT 000595649300005
関連URL isVersionOf https://doi.org/10.3892/ol.2020.12256
著者 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)|
キーワード Idiopathic pulmonary fibrosis High-resolution computed tomography Pirfenidone Forced vital capacity
備考 This fulltext is available in Feb. 2021.|
発行日 2020-02-23
出版物タイトル Respiratory Investigation
58巻
3号
出版者 Elsevier
開始ページ 185
終了ページ 189
ISSN 22125345
NCID AA12579673
資料タイプ 学術雑誌論文
言語 English
論文のバージョン author
PubMed ID 32102769
DOI 10.1016/j.resinv.2019.12.007
Web of Science KeyUT 000531841500009
関連URL isVersionOf https://doi.org/10.1016/j.resinv.2019.12.007
フルテキストURL BMCC19_1_1144.pdf
著者 Katsui, Kuniaki| Ogata, Takeshi| Watanabe, Kenta| Katayama, Norihisa| Soh, Junichi| Kuroda, Masahiro| Kiura, Katsuyuki| Maeda, Yoshinobu| Toyooka, Shinichi| Kanazawa, Susumu|
キーワード Induction chemoradiotherapy Lower lobe Mean lung dose Non-small cell lung cancer Radiation pneumonitis
発行日 2019-11
出版物タイトル BMC Cancer
19巻
1号
出版者 BMC
開始ページ 1144
ISSN 1471-2407
資料タイプ 学術雑誌論文
言語 English
OAI-PMH Set 岡山大学
著作権者 © The Author(s). 2019
論文のバージョン publisher
PubMed ID 31771538
DOI 10.1186/s12885-019-6359-9
Web of Science KeyUT 000499423900004
関連URL isVersionOf https://doi.org/10.1186/s12885-019-6359-9
著者 末久 弘| 豊岡 伸一| 堀田 勝幸| 内田 亜希子| 宗 淳一| 藤原 義朗| 松尾 恵太郎| 大内田 守| 高田 穣| 木浦 勝行| 伊達 洋至|
発行日 2008-12-01
出版物タイトル 岡山医学会雑誌
120巻
3号
資料タイプ 学術雑誌論文
著者 頼 冠名| 瀧川 奈義夫| 伊藤 佐智夫| 柏原 宏美| 市原 英基| 保田 立二| 清水 憲二| 谷本 光音| 木浦 勝行|
発行日 2012-12-03
出版物タイトル 岡山医学会雑誌
124巻
3号
資料タイプ 学術雑誌論文
著者 Murakami, Toshi| Takigawa, Nagio| Ninomiya, Takashi| Ochi, Nobuaki| Yasugi, Masaaki| Honda, Yoshihiro| Kubo, Toshio| Ichihara, Eiki| Hotta, Katsuyuki| Tanimoto, Mitsune| Kiura, Katsuyuki|
発行日 2014-01
出版物タイトル Lung Cancer
83巻
1号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/54499
フルテキストURL 70_4_243.pdf
著者 Osawa, Masahiro| Ohashi, Kadoaki| Kubo, Toshio| Ichihara, Eiki| Takata, Saburo| Takigawa, Nagio| Takata , Minoru| Tanimoto, Mitsune| Kiura, Katsuyuki|
抄録 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.
キーワード vandetanib VEGFR EGFR nonsmall cell lung cancer transgenic mouse
Amo Type Original Article
発行日 2016-08
出版物タイトル Acta Medica Okayama
70巻
4号
出版者 Okayama University Medical School
開始ページ 243
終了ページ 253
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2016 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 27549668
Web of Science KeyUT 000384748600003
JaLCDOI 10.18926/AMO/32669
フルテキストURL fulltext.pdf
著者 Takigawa, Nagio| Ohnoshi, Taisuke| Ueoka, Hiroshi| Kiura, Katsuyuki| Kimura, Ikuro|
抄録 <p>An etoposide-resistant subline, SBC-3/ETP, from a human small cell lung cancer cell line, SBC-3, was developed by continuous exposure to increasing concentrations of etoposide in culture. The SBC-3/ETP was 52.1-fold more resistant to etoposide than the parent cell line. The SBC-3/ETP was highly cross-resistant to teniposide, adriamycin, vinca alkaloids, 4-hydroperoxycyclophosphamide, CPT-11 and mitomycin C, and marginally cross-resistant to cisplatin, while the subline showed a collateral sensitivity to bleomycin. Topoisomerase I activity in the SBC-3/ETP was reduced to an extent of one half and topoisomerase II activity to an extent of one eighth in comparison with those of the SBC-3. Intracellular accumulation of [3H]-etoposide in the SBC-3/ETP was significantly lower in comparison to the SBC-3. An overexpression of MDR1 mRNA, and the presence of its product, P-glycoprotein, were detected in the SBC-3/ETP by Northern blotting and flowcytometry using a monoclonal antibody of the protein, MRK16. These results indicate that a decreased activity of topoisomerase II is the major factor for the development of etoposide resistance, and that an overexpression of the MDR1 gene is responsible, in part, for the development of resistance to the drug and some structurally unrelated compounds such as adriamycin and vinca alkaloids.</p>
キーワード small cell lung cancer etoposide-resistant cell line P-glycoprotein topoisomerase
Amo Type Article
発行日 1992-06
出版物タイトル Acta Medica Okayama
46巻
3号
出版者 Okayama University Medical School
開始ページ 203
終了ページ 212
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
PubMed ID 1354408
Web of Science KeyUT A1992JB50400009
JaLCDOI 10.18926/AMO/31626
フルテキストURL fulltext.pdf
著者 Matsushita, Akio| Tabata, Masahiro| Ueoka, Hiroshi| Kiura, Katsuyuki| Shibayama, Takuo| Aoe, Keisuke| Kohara, Hiroyuki| Harada, Mine|
抄録 <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>
キーワード drug screening system MTT assay lung cancer cell line drug resistance
Amo Type Article
発行日 1999-04
出版物タイトル Acta Medica Okayama
53巻
2号
出版者 Okayama University Medical School
開始ページ 67
終了ページ 75
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
論文のバージョン publisher
査読 有り
Web of Science KeyUT 000080058700002
JaLCDOI 10.18926/AMO/31598
フルテキストURL fulltext.pdf
著者 Kiura, Katsuyuki| Ohnoshi, Taisuke| Tabata, Masahiro| Shibayama, Takuo| Kimura, Ikuro|
抄録 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.
キーワード Adriamycin-resistant cell line MDR1 mRNA glutathione glutathione S-transferasse π DNA topoisomerase II
Amo Type Article
発行日 1993-06
出版物タイトル Acta Medica Okayama
47巻
3号
出版者 Okayama University Medical School
開始ページ 191
終了ページ 197
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 Copyright © 1999 Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 8104372
Web of Science KeyUT A1993LL12400008
関連URL http://ousar.lib.okayama-u.ac.jp/metadata/6296
著者 木浦 勝行|
発行日 1993-09-30
出版物タイトル
資料タイプ 学位論文