Causative connections between infections and cancer are ascertained for several types of viruses,
bacteria, and parasites. The mechanisms of cancer induction in chronically infected inflamed tissues
strongly implicate oxygen- and nitrogen-centered reactive species, and an impairment of redox-sensitive
molecular pathways involved in the tumorigenic transformation, tumor growth, altered immune defense,
and in the mechanisms of tumor cell death and survival. Here, we briefly reviewed mechanistic data on carcinogenesis and
tumor progression of three major infection-associated tumors, human papillomavirus-induced cervical cancer, hepatitis B
virus-positive hepatocarcinoma, and Helicobacter pylori-positive gastric cancer. Notwithstanding the contradictory results
of clinical studies on cancer chemoprevention with long-term, high dosage antioxidant vitamin/micronutrient supplementation,
natural and synthetic agents with proven capacity to affect redox-dependent molecular pathways still hold the
promise for preventing/delaying carcinogenesis initiation, as well as the overt malignancy evolution from dysplastic/
aplastic stages. Novel directions for a targeted antioxidant-based approach to the reduction of persistent infectiondriven
cancer risk stems from the current knowledge of critical factors in the host-microbe interaction leading to oncogenesis.
An emerging role of redox active substances in the chemotherapy of tumors relies on their stimulating effects towards
TRAIL-related apoptosis and the induction of intracellular oxidative stress.
Keywords: Antioxidants, Cervical cancer, Chemoprevention, Gastric adenocarcinoma, Hepatocarcinoma, Redox active compounds,
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