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Arch Dermatol. 2002;138:1429-1432.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

AGING, A COMPLEX process that defines those changes observed throughout the organism's life span, represents a biologic attrition at the cellular level resulting in cellular senescence and/or death. Aging is regarded by many as a cancer preventative mechanism,¹ as genomic DNA is continuously damaged by environmental insults as well as by internal oxidative metabolism and at the same time, DNA repair capacity deteriorates with age. If not properly repaired, DNA damage may lead to mutation formation in dividing cells and eventually to cancer.^2-3 Also, cumulative DNA damage would eventually interfere with appropriate gene and protein function resulting in failure of the cell to divide or perform its differentiated functions and leading to homeostatic failure.²

Indeed, a direct correlation was found between DNA repair capacity and the life span of the species,⁴ and an inverse correlation was found between life span and the organism metabolism.⁵ Thus, the aging process seems to . . . [Full Text of this Article]

CELLULAR SENESCENCE


TELOMERE SHORTENING AND SENESCENCE

TELOMERES AND DNA DAMAGE RESPONSES

MEDIATORS OF SENESCENCE OTHER THAN TELOMERE SHORTENING

HISTONE ACETYLATION AND SENESCENCE

THE SENESCENT PHENOTYPE

AGING AND LONGEVITY GENES

SUMMARY


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