FullText URL fulltext.pdf
Author Itano, Junko| Ohashi, Kadoaki| Senoo, Satoru| Oda, Naohiro| Nishii, Kazuya| Taniguchi, Akihiko| Miyahara, Nobuaki| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords Axillary lymphadenitis Mycobacterium avium complex infection Mycobacterium intracellulare
Published Date 2019
Publication Title Respiratory Medicine Case Reports
Volume volume28
Publisher Elsevier
Start Page 100947
ISSN 2213-0071
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2019 The Authors.
File Version publisher
PubMed ID 31681532
DOI 10.1016/j.rmcr.2019.100947
Web of Science KeyUT 000511444900001
Related Url isVersionOf https://doi.org/10.1016/j.rmcr.2019.100947
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
Author Ninomiya, Takashi| Takigawa, Nagio| Ichihara, Eiki| Ochi, Nobuaki| Murakami, Toshi| Honda, Yoshihiro| Kubo, Toshio| Minami, Daisuke| Kudo, Kenichiro| Tanimoto, Mitsune| Kiura, Katsuyuki|
Published Date 2013-05
Publication Title Molecular Cancer Therapeutics
Volume volume12
Issue issue5
Content Type Journal Article
JaLCDOI 10.18926/AMO/60796
FullText URL 74_5_371.pdf
Author Makimoto, Go| Ohashi, Kadoaki| Maeda, Yoshinobu| Kiura, Katsuyuki|
Abstract 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.
Keywords lung cancer anaplastic lymphoma kinase tyrosine kinase inhibitors resistance mechanism
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2020-10
Volume volume74
Issue issue5
Publisher Okayama University Medical School
Start Page 371
End Page 379
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2020 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 33106692
Web of Science KeyUT 000581970100001
NAID 120006892922
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
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 英語
File Version publisher
Refereed True
PubMed ID 8213217
Web of Science KeyUT A1993LV73800003
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
Publication Title Acta Medica Okayama
Published Date 2010-10
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/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
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 英語
File Version publisher
Refereed True
PubMed ID 1442149
Web of Science KeyUT A1992JL44200004
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
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 英語
File Version publisher
Refereed True
PubMed ID 12108583
Web of Science KeyUT 000176521200002
FullText URL fulltext.pdf
Author Harada, Daijiro| Isozaki, Hideko| Kozuki, Toshiyuki| Yokoyama, Toshihide| Yoshioka, Hiroshige| Bessho, Akihiro| Hosokawa, Shinobu| Takata, Ichiro| Takigawa, Nagio| Hotta, Katsuyuki| Kiura, Katsuyuki| Okayama Lung Cancer Study Group|
Keywords Alectinib anaplastic lymphoma kinase crizotinib drug therapy non-small cell lung carcinoma
Published Date 2021-01-20
Publication Title Thoracic Cancer
Volume volume12
Issue issue5
Publisher Wiley
Start Page 643
End Page 649
ISSN 1759-7706
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2021 The Authors.
File Version publisher
PubMed ID 33470536
DOI 10.1111/1759-7714.13825
Web of Science KeyUT 000608856400001
Related Url isVersionOf https://doi.org/10.1111/1759-7714.13825
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
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 英語
File Version publisher
Refereed True
PubMed ID 12530510
Web of Science KeyUT 000178668100007
FullText URL fulltext.pdf
Author Makimoto, Go| Misawa, Mahito| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords Chronic myeloid leukemia Chylothorax Dasatinib
Published Date 2022
Publication Title Respiratory Medicine Case Reports
Volume volume37
Publisher Elsevier
Start Page 101662
ISSN 2213-0071
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2022 The Authors.
File Version publisher
PubMed ID 35585905
DOI 10.1016/j.rmcr.2022.101662
Web of Science KeyUT 000807403400006
Related Url isVersionOf https://doi.org/10.1016/j.rmcr.2022.101662
FullText URL fulltext.pdf
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
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
FullText URL fulltext.pdf figure.pptx
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
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
FullText URL fulltext.pdf
Author Oda, Naohiro| Tabata, Masahiro| Uno, Masatoshi| Umeda, Yuzo| Kato, Hironari| Kubo, Toshio| Senoo, Satoru| Yagi, Takahito| Fujiwara, Toshiyoshi| Maeda, Yoshinobu| Kiura, Katsuyuki|
Keywords pancreas mucinous cystadenocarcinoma carboplatin paclitaxel
Published Date 2021-09-15
Publication Title Internal Medicine
Volume volume60
Issue issue18
Publisher The Japanese Society of Internal Medicine
Start Page 2967
End Page 2971
ISSN 0918-2918
NCID AA10827774
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
Copyright Holders © 2021 The Japanese Society of Internal Medicine
File Version publisher
PubMed ID 33814494
DOI 10.2169/internalmedicine.6730-20
Web of Science KeyUT 000697279400013
Related Url isVersionOf https://doi.org/10.2169/internalmedicine.6730-20
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
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 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
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
Publication Title Acta Medica Okayama
Published Date 2016-08
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
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
Publication Title Acta Medica Okayama
Published Date 1992-06
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