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Helicobacter pylori Infection – The Link Between Oxidative Damage, Cell Proliferation, Apoptosis, and Gastric Cancer

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Systems Biology of Free Radicals and Antioxidants

Abstract

The demonstration of the link between Helicobacter pylori (H. pylori) infection and gastritis, peptic ulcer, and gastric cancer is recognized as one of medicine’s most important breakthroughs. The complex network of bacterial, environmental, and host factors that modulate the natural history of the infection has been extensively investigated. Nevertheless, several key questions remain unanswered, such as who among the many infected patients will develop gastric cancer, why does the infection eventually lead to a benign or a malignant disease, and whether, apart from eradication, there are yet other methods of modulating risk. This chapter, apart from investigating in depth all the possible factors and mechanisms at play, is aimed at describing the scenario involving the role of oxidative DNA damage in prompting and modulating cell proliferation and apoptosis in gastric mucosa in correlation with bacterial virulence factors, DNA repair gene polymorphisms, and telomere dysfunction. Finally, this chapter describes the molecular and morphologic changes involved in the progression toward gastric precancerous and neoplastic gastric changes. The data summarized constitute sound evidence that gastric cancer is an “inflammatory cancer,” which develops in the context of H. pylori-related inflammation and whose development, progression, and invasion are supported by inflammation-related mechanisms.

Supported in part by grants from IARC (No. 1027) and MURST (No. 2005064071_002)

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Correspondence to Fabio Farinati .

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Farinati, F., Cardin, R., Piciocchi, M., Rodríguez-Castro, K., Maddalo, G., Rugge, M. (2014). Helicobacter pylori Infection – The Link Between Oxidative Damage, Cell Proliferation, Apoptosis, and Gastric Cancer. In: Laher, I. (eds) Systems Biology of Free Radicals and Antioxidants. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-30018-9_211

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