Abstract

Abstract Introduction: Fibroblast growth factors (FGFs) are potent mitogens and inducers of angiogenesis. FGF signalling pathway is closely associated with cancer development and progression. Fibroblast growth factor receptor 2 (FGFR2) gene, located at human chromosome 10q26, encodes FGFR2b and FGFR2c isoforms functioning as distinct FGF receptors. Gene amplification or missense mutation of FGFR2 occurs in gastric cancer (GC). Genetic alterations of FGFR2 may induce aberrant activation of FGFR2 signalling pathway, thereafter induce proliferation and survival of GC cells. FGFR2 plays an important role in gastric carcinogenesis. Patients and Methods: A total of 33 gastric cancer tissues with formalin-fixed, paraffin-embedded tumor slides were investigated by immunohistochemical staining with primary antibody against FGFR2. By Lauren's classification, there are 9 diffuse-type, 23 intestinal-type, and 1 mixed-type GC patients, respectively. Results: The FGFR2 immunohistochemical staining was classified as 0, 1+, 2+, and 3+ according to percentage of immunoreactive positive-staining FGFR2 cells in <10%, 10-25%, 25-50%, and >50% tumor cells, respectively. The relationship between the FGFR2 expression and the clinicopathological characteristics were analyzed. Among 33 GC patients, 13 patients (39.4%; 23-57%, 95% C.I.) had FGFR2 expression (1+, 2+, and 3+), and 11 patients (33.3%; 17-52%, 95% C.I.) had FGFR2 overexpression (2+ and 3+), respectively. FGFR2 expression was not correlated with diffuse-type versus intestinal-type GC patients (p=0.427, Fisher exact test). Conclusions: Overexpression of FGFR2 in gastric cancer forms the basis of the rational clinical application of future FGFR2-targeted cancer therapy for treatment of advanced GC. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 1770.

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