2014 Fiscal Year Final Research Report
Study for molecular basis of trastuzumab-resistance and the development of novel therapeutic strategies.
| Project/Area Number |
24591901
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Kansai Medical University (2013-2014)
Kyoto University (2012) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Eiji 京都大学, 医学研究科, 助教 (00612897)
SATO Fumiaki 京都大学, 医学研究科, 准教授 (20467426)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Keywords | 乳癌 / HER2 / トラスツズマブ / 耐性 / ＡＤＣＣ |
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| Outline of Final Research Achievements |
HER2-targeted therapy using trastuzumab has dramatically improved the prognosis of HER2-positive breast cancer. However, it becomes the important clinical issue how to overcome tastuzumab-resistant breast cancer. In this study, we addressed the molecular mechanism for acquired resistance to trastuzumab which can activate antibody dependent cell mediated cytotoxicity (ADCC). Gene expressing profile using ADCC-resistant breast cancer cell line showed that vacuolar type ATPase (vATPase) which drives active membrane transport was associated with ADCC-resistance. ATP6V1B1 gene coding subunit B1 might be specifically responsible for acquired resistance in terms of perforin/granzyme pathway.
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| Free Research Field |
乳腺外科学
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