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Abstract
Pathogenic and commensal microbes induce various levels of inflammation and metabolic disease in the host. Inflammation caused by infection leads to increased production of reactive oxygen species (ROS) and subsequent oxidative DNA damage. These in turn cause further inflammation and exacerbation of DNA damage, and pose a risk for cancer development. Helicobacter pylori-mediated inflammation has been implicated in gastric cancer in many previously established studies, and Fusobacterium nucleatum presence has been observed with greater intensity in colorectal cancer patients. Despite ambiguity in the exact mechanism, infection-mediated inflammation may have a link to cancer development through an accumulation of potentially mutagenic DNA damage in surrounding cells. The multiple DNA repair pathways such as base excision, nucleotide excision, and mismatch repair that are employed by cells are vital in the abatement of accumulated mutations that can lead to carcinogenesis. For this reason, understanding the role of DNA repair as an important cellular mechanism in combatting the development of cancer will be essential to characterizing the effect of infection on DNA repair proteins and to identifying early cancer biomarkers that may be targeted for cancer therapies and treatments.
Highlights
The significance of cancer as a disease that affects a large percentage of the world population is undeniable
The intrinsic pathway of genome alterations caused by infection is often linked to inflammation-mediated reactive oxygen species (ROS) production, which can increase the rate of genetic mutations that can accumulate to cause cancer (Hanahan and Weinberg, 2011)
ROS produced as a result of exposure of mouse mammary epithelial cells to MMP-3, a stromal enzyme that is linked to inducing epithelial-mesenchymal (EMT) transition and malignant transformation, caused activation of the transcription factor SNAIL, which induced oxidative DNA damage and EMT (Radisky et al, 2005)
Summary
The significance of cancer as a disease that affects a large percentage of the world population is undeniable. Chronic inflammation from infection causes abnormal immune response, obesity, DNA damage and cancer. Bacterial infections increase cancer risk through either an extrinsic pathway, linked to induction of chronic inflammatory diseases that can increase cancer risk, or an intrinsic pathway, which is the accrual of genetic mutations that cause inflammation and transformation (Mantovani et al, 2008). The intrinsic pathway of genome alterations caused by infection is often linked to inflammation-mediated reactive oxygen species (ROS) production, which can increase the rate of genetic mutations that can accumulate to cause cancer (Hanahan and Weinberg, 2011). We will bring the link of Helicobacter pylori with gastric cancer and microbial infection associated colorectal cancer under the scope of DNA damage repair following infection. The innate and adaptive immune responses will be discussed
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