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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Journal of Environmental Pathology, Toxicology and Oncology
Импакт фактор: 1.625 5-летний Импакт фактор: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN Печать: 0731-8898
ISSN Онлайн: 2162-6537

Выпуски:
Том 39, 2020 Том 38, 2019 Том 37, 2018 Том 36, 2017 Том 35, 2016 Том 34, 2015 Том 33, 2014 Том 32, 2013 Том 31, 2012 Том 30, 2011 Том 29, 2010 Том 28, 2009 Том 27, 2008 Том 26, 2007 Том 25, 2006 Том 24, 2005 Том 23, 2004 Том 22, 2003 Том 21, 2002 Том 20, 2001

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2017019476
pages 131-150

DNA Double-Strand Breaks Caused by Different Microorganisms: A Special Focus on Helicobacter pylori

Pinar Erkekoglu
Hacettepe University, Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Ankara, Turkey
Didem Oral
Hacettepe University, Faculty of Pharmacy, Department of Pharmaceutical Toxicology, Ankara, Turkey
Belmar Kocer-Gumusel
Hacettepe University, Faculty of Pharmacy, Department of Toxicology, 06100 Ankara, Turkey
Ming-Wei Chao
Chung Yuan Christian University, Department of Bioscience Technology, Zhongli district, Taoyuan, Taiwan

Краткое описание

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.


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