Recent advances in molecular biology lead to a better understanding of the carcinogenesis of gastric cancer. It is the accumulation of multiple gene abnormalities that result in the transformation of a normal epithelial cell to a malignant cell. Progressive accumulations of genetic changes have been evidenced in the different stages of Correa’s model. Microsatellite instability and telomerase reactivation occurred in early carcinogenesis. Mutation of p53 and adenomatous polyposis coli genes, and amplification and overexpression of c-myc and cyclin E genes are found in advanced gastric cancer. Unlike colon and pancreatic cancers, gastric cancer rarely involves k-ras mutation. Multiple autocrine and paracrine loops interact with each other in the progression of advanced gastric cancer. These include hepatocyte growth factor and the c-met gene; fibroblast growth factor and the k-sam gene; epidermal growth factor and the c-erbB-2 or HER-2/neu genes; and epidermal growth factor (EGF)/transforming growth factor-alpha and EGF receptors. In addition, E-cadherin, and CD44 have been shown to play an important role in metastasis. Find best deals online – cialis professional can be available every time you visit.