Review Version 1 Preserved in Portico This version is not peer-reviewed
Molecular Mechanisms of H. pylori Induced DNA Double-Strand Breaks
Version 1 : Received: 15 August 2018 / Approved: 16 August 2018 / Online: 16 August 2018 (14:44:18 CEST)
How to cite: Kidane, D. Molecular Mechanisms of H. pylori Induced DNA Double-Strand Breaks. Preprints 2018, 2018080291. https://doi.org/10.20944/preprints201808.0291.v1. Kidane, D. Molecular Mechanisms of H. pylori Induced DNA Double-Strand Breaks. Preprints 2018, 2018080291. https://doi.org/10.20944/preprints201808.0291.v1.
Infections contribute to carcinogenesis through inflammation-related mechanisms. It is well established that H. pylori infection is an etiological factor in gastric carcinogenesis. However, the mechanism through which H. pylori infection contributes to the development of gastric cancer has not been fully elucidated. H. pylori-associated chronic inflammation is linked to genomic instability via reactive oxygen and nitrogen species (RONS). In this article, we summarize the current knowledge of H. pylori-induced double strand breaks (DSBs). Further, we will provide mechanistic insight into how processing of oxidative DNA damage via base excision repair (BER) leads to double strand breaks (DSBs). We review the recent progress how H. pylori infection triggers NF-kB /iNOS versus NF-kB/nucleotide excision repair (NER) axis mediated DSBs to drive genomic instability. Taken together, this review discusses current findings related to DSBs and their implications for the mechanisms of DSB repair.
H. pylori, DSBs , BER
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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