AIM: The aim of this study is to identify the AKT1 gene mutation driven pathogenicity in gastric cancer for Mizo population. METHODS: 50 diffuse-type gastric tumors were analyzed for AKT1 exon 2 and 14 mutations. Cell-cycle aberration was analyzed in the AKT1-mutated samples and the stability of the protein as well as exonic splicing enhancer motifs were examined. RESULTS: The novel mutations, 15553T >A and 25376C >G might affect the exonic splicing enhancers and silencers. Significant decline was observed in the S-phase population in the tumor cells with 15553T >A and 15579G >C mutations suggesting the arrest of G1 phase. CONCLUSION: The present study is a novel finding of the possible role of AKT1 mutations which might help to identify gastric cancer patients.
AIM: The aim of this study is to identify the AKT1 gene mutation driven pathogenicity in gastric cancer for Mizo population. METHODS: 50 diffuse-type gastric tumors were analyzed for AKT1 exon 2 and 14 mutations. Cell-cycle aberration was analyzed in the AKT1-mutated samples and the stability of the protein as well as exonic splicing enhancer motifs were examined. RESULTS: The novel mutations, 15553T >A and 25376C >G might affect the exonic splicing enhancers and silencers. Significant decline was observed in the S-phase population in the tumor cells with 15553T >A and 15579G >C mutations suggesting the arrest of G1 phase. CONCLUSION: The present study is a novel finding of the possible role of AKT1 mutations which might help to identify gastric cancerpatients.