2015 Fiscal Year Final Research Report
Analysis of resistance mechanism to amrubicin
Project/Area Number |
25461158
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Respiratory organ internal medicine
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Research Institution | Kobe University |
Principal Investigator |
Tachihara Motoko 神戸大学, 医学(系)研究科(研究院), 助教 (40448626)
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Co-Investigator(Kenkyū-buntansha) |
NISHIMURA YOSHIHIRO 神戸大学, 医学部附属病院, 教授 (20291453)
KOBAYASHI KAZUYUKI 神戸大学, 大学院医学研究科, 講師 (50403275)
TAMURA DAISUKE 神戸大学, 医学部附属病院, 特定助教 (80646597)
NAGANO TATSUYA 神戸大学, 大学院医学研究科, 特命助教 (80624684)
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Project Period (FY) |
2013-04-01 – 2016-03-31
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Keywords | アムルビシン / 薬剤耐性 / アンフィレグリン |
Outline of Final Research Achievements |
Amrubicin (AMR) has shown promising activity for lung cancer. However, little is known about the mechanism of resistance for this agent. Transcriptome analysis of amrubicinol (AMR-OH)-resistant lung cancer cell lines (H520/R, and DMS53/R) showed that amphiregulin (AREG) was most highly up-regulated gene in both of the AMR-OH-resistant cells compared to H520 and DMS53. AREG concentration in cultured medium of DMS53/R was higher compared to DMS53 after 72h culture with AMR-OH. A conditioned medium from DMS53/R decreased sensitivity to AMR-OH in DMS53. On the other hand, DMS53/R transfected with siRNA directed against AREG recovered sensitivity to AMR-OH. Additional administration of cetuximab (CET) on AMR-OH also recovered sensitivity to AMR-OH in DMS53/R. AMR/CET treatment showed higher antitumor activity in DMS53/R-bearing mice than AMR treatment.
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Free Research Field |
呼吸器内科
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