Background: Cancer is considered a major cause of death worldwide. The etiology of cancer is linked
to environmental and genetic inheritance causes. Approximately 90 percent of all human cancers have an environmental
cause (non-genetic inheritance) predominantly through lifestyle choices (smoking, diet, UV radiation)
while the remaining due to infections and chemical exposure. Cancer is a multistage process that involves mutational
changes and uncontrolled cell proliferation. Research has firmly established a causal and contributory role
of oxidative stress and oxidative damage in cancer initiation and progression.
Methods: The purpose of this article is to review the role that oxidative stress and reactive oxygen species play in
the development of cancer. Both endogenous and exogenous sources of reactive oxygen species result in increased
oxidative stress in the cell. Excess reactive oxygen fumed can result in damage to and modification of
cellular macromolecules most importantly genomic DNA that can produce mutations. In addition, oxidative stress
modulates gene expression of downstream targets involved in DNA repair, cell proliferation and antioxidants. The
modulation of gene expression by oxidative stress occurs in part through activation or inhibition of transcription
factors and second messengers. The role of single nuclear polymorphism for oxidative DNA repair and enzymatic
antioxidants is important in determining the potential human cancer risk.
Conclusion: oxidative stress and the resulting oxidative damage are important contributors to the formation and
progression of cancer.