© 2003 Blackwell Publishing Ltd, Helicobacter , 8 (Suppl. 1), 44–52 44 Volume 8 • Supplement 1 • 2003 HELICOBACTER Blackwell Publishing Ltd. Helicobacter pylori and gastric malignancies Gerardo Nardone * and Andrea Morgner † * Departments of Clinical and Experimental Medicine, Gastroenterology Unit, University of Naples Federico II, Naples, Italy, † Medical Department 1, Hematology, Oncology, and Gastroenterology, University Hospital Dresden, Dresden, Germany ABSTRACT Despite decreasing incidence during the last 50 years, gastric cancer still ranks as one of the most frequent cancers. A multifactorial model of human gastric carcinogenesis is currently accepted in which different dietary and nondietary factors, including genetic susceptibility of the host and Helicobacter pylori infection are involved at different stages in the cancer process. On the molecular level, at least two pheno- types, associated with distinct pathways of genome destabilization, have been identified. However, app- lying new technologies such as cDNA microarrays a new era in the analysis of molecular markers has started. This molecular technology may open the path towards novel treatment modalities, i.e. gene therapy. Epidemiological, biological, and molecular genetic studies have also implicated the role of H. pylori in lymphomagenesis. Knowledge of pathogenesis and therapy is increasing while good epidemiological data are rare. Many studies have demonstrated that MALT- type lymphomas develop along two different pathways: t(11;18)-positive cases, and t(11;18)-negative cases. Meanwhile, a third translocation could be detected, the t(14;18), opening the discussion of a possible third pathway of lymphoma development. Keywords. Helicobacter pylori, gastric cancer, gas- tric lymphoma, epidemiology, pathogenesis, therapy. T his review is a selection of studies on gastric cancer and gastric lymphoma published in MEDLINE from April 2002 to April 2003 rep- resenting advances in knowledge of epidemiology, pathogenesis, molecular alteration, Helicobacter pylori relationship and therapy. Gastric cancer Epidemiology Gastric cancer still ranks as one of the most fre- quent cancers and remains a public health concern because of its high-case-fatality rate, poor prog- nosis and limited treatment options. The incidence of gastric cancer varies considerably worldwide occurring more frequently in deve- loping than in industrialized countries, and tends to show a predilection for urban and lower socioeconomic groups. Newnham et al. reviewed the epidemiology and mortality of gastric cancer from 1971 to 1999 in England and Wales using cancer registration data. The age standardized incidence of gastric cancer decreased from 31.8 to 18.9 per 100,000 men, and from 15.1 to 7.3 per 100,000 women. The age standardized relative survival was significantly higher in women than in men: after 5 years 7.7% of men and 8.4% of women were still alive [1,2]. Environmental factors, diet and smoking Environmental factors, particularly diet, play an important role in the pathogenesis of gastric can- cer. Diet rich in complex carbohydrates, salted, pickled or smoked foods, dried fish, and cooking oil has been linked with an increased risk while diet rich in fresh fruit and vegetables has been associated with a low risk of gastric cancer [3]. In a large population-based prospective study with a 10-year follow-up, the relative risk for the deve- lopment of gastric cancer associated with fruit and vegetable intake 1 or more days per week compared to less than 1 day per week was 0.64 (95% CI 0.45 – 0.92) for yellow vegetable, 0.48 (95% CI 0.25 – 0.89) for white vegetable, and 0.70 (95% CI 0.49 – 1.00) for fruit [4]. Thus, vegetable and fruit intake even in low amount, is associated with a lower risk of gastric cancer. The risk of gastric cancer did not vary substantially according Correspondence: Andrea Morgner, University Hospital Dresden, Medical, Department I, Hematology, Oncology & Gastroenterology, Fetscherstrasse 74, 01307 Dresden, Germany. Tel. +49 351458 4702; Fax: +49 351458 4394; E-mail: morgner@mk1.med.tu-dresden.de