[Exome sequencing of gastric cancers screened the differences of clinicopathological phenotypes between the mutant and the wide-type of frequently mutated genes].

Objective To discover frequently mutated new gastric cancer-related genes by exome sequencing technology and to analyze mutated their relationships with different clinicopathological phenotypes of gastric cancer. Methods Tumor samples of gastric cancers and preoperative peripheral blood samples from 30 patients were collected respectively from January to March, 2016 in the department of general surgery, Chinese PLA General Hospital. Exome sequencing on samples were performed. Using peripheral bloods as control, mutations in tumor samples were discovered by Mutect and Varscan. Frequently mutated gastric cancer-related genes were defined as genes mutated more frequently than TP53. Difference between the mutant and wild-type of certain genes were compared on common clinicopathological phenotypes, such as age, gender, tumor position, differentiation, metastasis lymph nodes, etc. Results There were 27 frequently mutated genes were founded, most of which showed no relationship with clinicopathological phenotypes of gastric cancer. Cases with mutant and wild-type TAS2R43 showed statistically significant difference in gastric body cancer(55.6% vs 9.5%, P=0.022). Cases with mutant and wild-type ANKRD36C showed statistically significant difference in gastric body cancer (62.5% vs 9.1%, P=0.005). Cases with mutant and wild-type ANKRD36 showed statistically significant difference in proximal gastric cancer (8.33% vs 44.4%, P=0.049). Cases with mutant SYNE1 suffer from less metastatic lymph nodes than those with wild types(2.1±2.4 vs 8.8±9.5, P=0.006). Cases with mutant ADAR are younger than those with wild types(50.7±11.5 year vs 64.0±9.8 year, P=0.006). Conclusion Mutant TAS2R43, ANKRD36 and ANKRD36C were related to location of gastric cancer. Mutant SYNE1 was related to gastric cancer with less lymph nodes metastasis. Mutant ADAR may lead to gastric cancers in younger groups. Key words: Whole exome sequencing; Gastric cancer; Mutation; Phenotype