[Frontiers in Bioscience 14, 1490-1504, January 1, 2009]
Helicobacter Pylori associated global gastric cancer burden
Sam M. Mbulaiteye1, Michie Hisada2, Emad M. El-Omar3
1Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, 2TAP Pharmaceutical Products Inc, Lake Forest, Illinois, 3Aberdeen University and Aberdeen Royal Infirmary, Aberdeen, Scotland, UK
TABLE OF CONTENTS
Helicobacter pylori infection is ubiquitous, infecting close to one-half of the world's population, but its prevalence is declining in developed countries. Chronic H. pylori infection is etiologically linked to gastric adenocarcinoma, especially non-cardia type (63% of all stomach cancer or ~5.5% of the global cancer burden: ~25% of cancers associated with infectious etiology), and to gastric mucosal associated lymphoid tissue (MALT) lymphoma, which accounts for up to 8% of all non-Hodgkin lymphoma. Epidemiological, clinical, and animal studies have established a central role for H. pylori in gastric carcinogenesis and provided insights into the mechanisms and biologic relationships between bacterial infection, host genetics, nutrition, and environmental factors. These discoveries invite strategies to prevent infection to be the logical primary goals in a multi-pronged effort to curtail suffering and death from H. pylori infection-associated cancers.