ライブラリ登録: Guest
Begell Digital Portal Begellデジタルライブラリー 電子書籍 ジャーナル 参考文献と会報 リサーチ集
Journal of Environmental Pathology, Toxicology and Oncology
インパクトファクター: 1.625 5年インパクトファクター: 1.63 SJR: 0.402 SNIP: 0.613 CiteScore™: 2.3

ISSN 印刷: 0731-8898
ISSN オンライン: 2162-6537

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

要約

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.


Articles with similar content:

A Review of Molecular Events of Cadmium-Induced Carcinogenesis
Journal of Environmental Pathology, Toxicology and Oncology, Vol.33, 2014, issue 3
Chendil Damodaran, Joe Luevano
The Identification and Development of Specific Monoclonal Antibodies to Squamous Cell Carcinoma
Critical Reviews™ in Immunology, Vol.21, 2001, issue 1-3
Joyce Wolf, Joseph Scherrer, Myron Arlen, Al Tsang, Olga Saric
Chemokines in Respiratory Viral Infections: Focus on Their Diagnostic and Therapeutic Potential
Critical Reviews™ in Immunology, Vol.31, 2011, issue 4
Stavros Apostolakis, Demetrios A. Spandidos, Virginia Amanatidou, Apostolos Zaravinos
Alterations in Cell Proliferation Related Gene Expressions in Gastric Cancer
Critical Reviews™ in Eukaryotic Gene Expression, Vol.21, 2011, issue 3
Kyung-Hee Chun, In-Hoo Kim, Pann-Ghill Suh, Kyungtae Kim
Major Histocompatibility Complex Class I Molecules and Resistance against Intracellular Pathogens
Critical Reviews™ in Immunology, Vol.14, 1994, issue 3-4
Gabriel Gachelin, Christiane Delarbre, David M. Ojcius, Philippe Kourilsky