ABSTRACT
Gastric cancer is a leading cause of cancer death worldwide and is responsible for the majority of cancer-related deaths in developing countries. The vast majority of gastric cancers form as the consequence of sporadic genetic alterations that occur in the gastric epithelium of individuals who have no inherent predisposition to gastric cancers. The sporadic gastric adenocarcinomas arise as the result of the accumulation of these genetic alterations that cause the neoplastic transformation of gastric epithelium. Alterations appear to underlie a multistage process of carcinogenesis that results in normal gastric epithelial cells transforming into gastric adenocarcinoma cells. STK11 was recently cloned from the locus linked to Peutz-Jeghers syndrome. This syndrome is characterized most prominently by gastrointestinal hamartomatous polyps and melanocytic macules of the lips, buccal mucosa, and digits. HST-1 was identified as a transforming gene from studies that involved transfecting NIH-3T3 cells with DNA samples from gastric carcinomas and adjacent non-neoplastic gastric mucosa.
