DNA damage and mitochondria in cancer and aging

Age and DNA repair deficiencies are strong risk factors for developing cancer. This is reflected in the comorbidity of cancer with premature aging diseases associated with DNA damage repair deficiencies. Recent research has suggested that DNA damage accumulation, telomere(definition) dysfunction and the accompanying mitochondrial dysfunction(definition) exacerbate the aging process and may increase the risk of cancer development. Thus, an area of interest in both cancer and aging research is the elucidation of the dynamic crosstalk between the nucleus and the mitochondria. In this review, we discuss current research on aging and cancer with specific focus on the role of mitochondrial dysfunction in cancer and aging as well as how nuclear to mitochondrial DNA damage signaling may be a driving factor in the increased cancer incidence with aging. We suggest that therapeutic interventions aimed at the induction of autophagy(definition) and mediation of nuclear to mitochondrial signaling may provide a mechanism for healthier aging and reduced tumorigenesis.