Telomere Dysfunction and DNA Damage Checkpoints in Diseases and Cancer of the Gastrointestinal Tract

Aging occurs after the reproductive phase of life has been completed. The aging process is associated with a progressive decline in organ maintenance and an increasing risk of diseases, particularly cancer. A current hypothesis indicates that aging is not programmed, but rather is the result of stochastic interaction consisting of the injury and repair processes competing with other organismal functions—such as learning, motor activity, and reproduction—for energy resources that are necessary to maintain the integrity of molecular structures.1 According to this model, the failure of cellular and tissue maintenance and repair results from integrated actions among genes, the environment, and intrinsic defects of the organism. This finally leads to an accumulation of molecular damage. Among the various types of molecular damage, the accumulation of nuclear DNA damage seems to be an important factor of human aging.2 Different mechanisms may contribute to this accumulation, including oxidative metabolites, such as reactive oxygen species (ROS), irradiation, and telomere shortening.