DNA double-strand breaks caused by different microorganisms: A special focus on helicobacter pylori


ERKEKOĞLU Ü. P., Oral D., GÜMÜŞEL B., Chao M.

Journal of Environmental Pathology, Toxicology and Oncology, vol.36, no.2, pp.131-150, 2017 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 36 Issue: 2
  • Publication Date: 2017
  • Doi Number: 10.1615/jenvironpatholtoxicoloncol.2017019476
  • Journal Name: Journal of Environmental Pathology, Toxicology and Oncology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.131-150
  • Keywords: DNA damage, double-strand DNA break, gastric cancer, Helicobacter pylori, inflammation, reactive oxygen species, CYTOLETHAL DISTENDING TOXIN, NITRIC-OXIDE SYNTHASE, GASTRIC EPITHELIAL-CELLS, OXIDATIVE STRESS, REACTIVE OXYGEN, VACUOLATING CYTOTOXIN, PROMOTER METHYLATION, INCREASED EXPRESSION, CHRONIC INFLAMMATION, DAMAGE RESPONSE
  • Lokman Hekim University Affiliated: No

Abstract

© 2017 Begell House, Inc.The association between inflammation and cancer has long been recognized. Several studies have found that different types of tumors develop at sites of chronic inflammation. It is stated that over 15%–20% of malignancies worldwide can be related to infections caused by viruses, bacteria, and schistosomes. Inflammatory conditions are characterized by overexpression of inducible nitric oxide synthase (iNOS) and overproduction of nitric oxide/reactive nitrogen species (ROSs/RNSs) in epithelial cells. Reactive oxygen species (ROSs) may also lead to cellular alterations and eventually to inflammation. A variety of chronic infectious diseases can generate steady-state levels of ROSs/RNSs within infected cells and possibly lead to different types of DNA lesions. Accumulation of DNA lesions may finally lead to mutations that may activate oncogenes or inactivate tumor suppressor genes. Helicobacter pylori has been shown to generate ROSs/RNSs, induce DNA damage, and lead to chronic inflammation in gastric epithelial cells. A limited number of studies have addressed the effects of Helicobacter pylori on DNA damage, particularly its impact on single-strand and double-strand DNA breaks. This bacterium is classified as a Group I carcinogen by the International Agency for Research on Cancer on the basis of numerous animal and epidemiological studies. Chronic Helicobacter pylori infection can lead to increased risk of gastric cancer and mucosa-associated lymphoid tissue (MALT) lymphoma. This review addresses the DNA-damaging and double-strand break–inducing effects of different microorganisms and their toxins, specifically focusing on Helicobacter pylori.