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Helicobacter pylori and Cytokines in the Genesis of Gastric Cancer

  • Chapter
Cytokines in the Genesis and Treatment of Cancer

Part of the book series: Cancer Drug Discovery and Development ((CDD&D))

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Abstract

Rudolph Virchow pioneered the hypothesis that inflammation exerts a profound influence on the development and biological behavior of cancer nearly 150 years ago, and since that time it has become increasingly apparent that microbial pathogens contribute to the genesis of a substantial number of malignancies worldwide (1). Conservative estimates indicate that nearly 15% of all cancer cases are attributable to infectious agents, translating to a malignant burden of 1.2 million cases per year (1). One mechanism that contributes to carcinogenesis induced by chronic pathogens is the concomitant inflammatory response that leads to the production of mutagenic substances, such as nitric oxide (2). Nitric oxide, in turn, can be converted to reactive nitrogen species, which nitrosylate a variety of cellular targets including DNA and proteins, and similarly, Superoxide anion radicals generated by polymorphonuclear cells induce DNA damage through the formation of DNA adducts. Viral agents can directly transform host cells by integrating active oncogenes into the host genome (1). Thus, there is precedence and support for the concept that infectious agents can initiate or promote pathways that eventuate in neoplasia.

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Peek, R.M. (2007). Helicobacter pylori and Cytokines in the Genesis of Gastric Cancer. In: Caligiuri, M.A., Lotze, M.T. (eds) Cytokines in the Genesis and Treatment of Cancer. Cancer Drug Discovery and Development. Humana Press. https://doi.org/10.1007/978-1-59745-455-1_1

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