Sa1949 Validity of Serum Markers As Non-Endoscopic Screening Method for Gastric Cancer

Abstract

of malignant GIST. Methods From October 2008 to September 2013, we collected consecutively 58 samples of GISTs. Out of them, we selected 14 malignant GISTs and 37 low risk ones which represent slow-growth. Clinical or molecular characteristics were compared with each other. Mutation of c-kit or PDGFRA was analyzed by Direct-sequencing. Quantitative expression of c-kit, PDGFRA and ETV1 were evaluated by a real-time PCR. Results Regarding Clinical parameters, the mean tumor size was larger at malignant GIST (118±78mm) than low risk GIST (27±12mm). The prevalence of Gastric GIST was lower at malignant GIST (9/14; 64%) than low risk GIST (35/37; 94%). In mutation analysis, mutation status was different from each group. Notably, wild type and point mutation of c-kit exon 13 were observed only in malignant GIST. On the other hand, point mutation of c-kit exon 11 and PDGFRA exon18 were all belonged to low risk GIST. Loss of heterozygosity was observed only at two malignant GISTs. Expression of c-kit, PDGFRA and ETV1 was significantly lower at malignant GIST than low risk GIST, respectively. In univariate analysis, low c-kit expression, mutation type and tumor location were significant factors of malignant GIST. Multivariate analysis showed that low c-kit expression is the only factor to predict malignant (odds ratio: 9.2 (2.1-39.7)). Conclusion In addition to conventional malignant factors like tumor size and location, genetic factors (mutation, LOH and c-kit expression) have a possibility to decide GIST progression.