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.