Development of FGFR2 targeting therapy for the patients with EGJ adenocarcinoma.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25861203
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Digestive surgery
• Research Institution: Japanese Foundation for Cancer Research (2015); Kyushu University (2014); Kumamoto University (2013)
• Principal Investigator: Imamura Yu 公益財団法人がん研究会, その他部局等, 医員 (70583045)
• Co-Investigator(Renkei-kenkyūsha): BABA Hideo 熊本大学, 消化器外科, 教授 (20240905)
• Research Collaborator: TOKUNAGA Ryuma
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 食道胃接合部腺癌 / FGFR2 / 予後 / 遺伝子増幅

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.

Free Research Field

食道胃接合部腺癌