Persistent infection with Helicobacter pylori and the development of gastric cancer.
Gastric malignancies have been closely linked to infection of the gastric mucosa with Helicobacter pylori, but the individual factors involved in the multistage process of tumor development are still poorly understood. H. pylori evades the host defense system and causes persistent infection and chronic inflammation. Immune activation leads to DNA damage by the release of oxygen and nitrogen radicals. Ongoing tissue repair mechanisms and the secretion of cytokines and growth factors, as well as bacterial effector molecules, cause disturbances in the balance between epithelial cell proliferation and apoptosis, promote the accumulation of potential oncogenic mutations, and support neovascularization and tumor growth. In addition, H. pylori might hamper the development of an efficient antitumor immunity and provoke immune-mediated pathology. This review summarizes the recent progress in the understanding of the intimate bacteria-host relationship and the mechanisms by which H. pylori may promote the process of tumor development.
Normark
Staffan
S
Microbiology and Tumor Biology Center and Smittskyddsinstitutet, Karolinska Institutet, Stockholm, Sweden.
Nilsson
Christina
C
Normark
Birgitta Henriques
BH
Hornef
Mathias W
MW
D017209:Apoptosis; D004249:DNA Damage; D005753:Gastric Mucosa / Q000382:microbiology*; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D018384:Oxidative Stress; D013274:Stomach Neoplasms / Q000382:microbiology*