Helicobacter pylori is a common bacterial pathogen that colonizes the gastric mucosa of over 50% of the world's population. All infected individuals exhibit chronic gastric inflammation, and approximately 1% of patients develop gastric cancers, including adenocarcinomas and mucosal-associated lymphoid tissue lymphomas. In 1994, the World Health Organization International Agency for Research on Cancer classified H. pylori as a type I, or definite carcinogen. Because the prevalence of gastric cancers among H. pylori-infected patients varies between individuals, countries, and geographic areas, H. pylori disease-related outcomes are believed to be determined by an interplay between host factors, bacterial factors, and their interaction with the environment. This review highlights recent advances in our knowledge on H. pylori disease pathogenesis, focusing on the role of the host, bacteria, and environment in the development of gastric carcinoma.