This review summarizes the significant recent advances in our understanding of the clinical, epidemiologic, and pathologic aspects of gastric adenocarcinoma, gastrointestinal stromal tumors (GISTs), and mucosa-associated lymphoid tissue (MALT) lymphoma. Most of the advances in distal gastric adenocarcinoma are in its etiology and pathogenesis. The modulation of the inflammatory response to Helicobacter pylori organisms has been determined to be at the center of the precancerous process. These advances in the understanding of the pathogenesis of H. pylori-related carcinogenesis are relevant to the design of prevention strategies in high-risk populations. New markers of GISTs have focused on the cell of origin and have made possible the development and monitoring of new drugs that are effective even in metastatic tumors. MALT lymphomas have been causally associated with H. pylori infection. Molecular markers are useful to distinguish tumors that respond to H. pylori eradication from those requiring classic chemotherapy.