Over the past year Helicobacter pylori has been confirmed as the most important risk factor for non-cardia gastric adenocarcinomas and gastric mucosa-associated lymphoid tissue (MALT) lymphomas. Eradication therapy has been proven to be beneficial when given prior to the development of intestinal metaplasia, but is less efficacious when administered later. However, the best data from clinical trials indicate that H. pylori eradication alone will have only a moderate effect on gastric cancer incidence worldwide. The mechanisms responsible for H. pylori-associated gastric carcinogenesis continue to be dissected. Accumulating evidence suggests that some H. pylori may be able to invade through the gastric epithelial barrier, though pro-carcinogenic effects may also be related to the complex and evolving pathways of altering signal transduction pathways within gastric epithelial cells that are stimulated by adherence and translocation of H. pylori products through its type IV secretory system. Determinants of the host response to H. pylori infection continue to focus on polymorphisms in genes related to the innate and acquired immune responses, including NOD2, COX-2, and TLR-4. H. pylori eradication is indicated for low-grade gastric B-cell MALT lymphoma and may even provide "cure" in some apparently H. pylori-negative cases. How and why does H. pylori promote lymphomagenesis? Some evidence from human and murine models points to specific chromosomal translocations and host genetic polymorphisms as relating to the outcome of infection. Finally, Helicobacter hepaticus infection has been linked to both intestinal and breast tumorigenesis in susceptible strains of female mice - a provocative and novel finding warranting further investigation.