Crosstalk Between DNA Damage and Inflammation in the Multiple Steps of Gastric Carcinogenesis

摘要: Over the last years, intensive investigations in molecular biology and cell physiology extended tremendously knowledge about association of inflammation cancer. In frame this paradigm, human pathogen Helicobacter pylori triggers gastritis gastric ulcer disease, contributes to development Mechanisms, by which bacteria-induced mucosa leads intestinal metaplasia carcinoma, are represented review. An altered cell-signaling response increased production free radicals epithelial immune cells account for accumulation DNA damage mucosa, if infection stays untreated. Host genetics environmental factors, especially diet, can accelerate process, offers opportunity intervention based on a balanced nutrition. It is supposed that might influence stem- or progenitor tissue predisposing tumor relapse. Herein, strongly mutated labile, restricts therapy options. Thus, understanding mechanisms underlie carcinogenesis will be preeminent importance strategies screening early detection. As most cancer patients face late-stage disease with poor overall survival, multi-targeted therapeutic major challenge future.