| Project/Area Number |
25861203
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Digestive surgery
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| Research Institution | Japanese Foundation for Cancer Research (2015)
Kyushu University (2014)
Kumamoto University (2013) |
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Principal Investigator |
Imamura Yu 公益財団法人がん研究会, その他部局等, 医員 (70583045)
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| Co-Investigator(Renkei-kenkyūsha) |
BABA Hideo 熊本大学, 消化器外科, 教授 (20240905)
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| Research Collaborator |
TOKUNAGA Ryuma
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 食道胃接合部腺癌 / FGFR2 / 予後 / 遺伝子増幅 / 悪性度 / コピー数 / Ampification / 食道胃接合部癌 / 食道腺癌 / 分子標的治療 |
|---|
| Outline of Final Research Achievements |
We hypothesized that FGFR2 amplification is associated with FGFR2 expression, resulting in tumor growth and poorer outcome in esophagogastric junction (EGJ) adenocarcinoma. FGFR2 amplification and FGFR2 IHC expression were 15% and 61%, respectively.Although these two statuses were significantly correlated (P < 0.05), only FGFR2 IHC expression was significantly associated with tumor depth (P < 0.001) and
overall survival of patients (univariate P = 0.007). Supporting these findings, FGFR2 overexpression was associated with tumor cell proliferation, cell cycle progression,and anti-apoptosis. Selective inhibition of FGFR2 sufficiently suppressed tumor cell proliferation. FGFR2 amplification was significantly associated with FGFR2 expression. FGFR2 expression (but not FGFR2 amplification) was associated with tumor growth and patient outcomes. Our findings support FGFR2 as a novel therapeutic target for EGJ adenocarcinoma.
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