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The aging process that takes place in normal somatic cells and the natural limit on the number of times such cells can undergo mitosis involve a sequential shortening of telomeres due to failure of terminal sequences to be replicated during mitosis. Cells in which this shortening does not occur (cancer cells, germ cells, hematopoietic stem cells, and others) display a transient expression of telomerase, which not only delays the erosion of telomeres but actually adds DNA bases to telomeres. Experimental transfection of a gene for the catalytic component of telomerase into normal, aging cells results in extension of telomeres. Restoring telomere length appears to reset gene expression, cell morphology, and the replicative life span. It has therefore been suggested that such procedures may permit therapeutic modification of the cellular mechanisms underlying age-related diseases such as atherosclerosis, osteoarthritis, macular degeneration, and Alzheimer dementia. Cellular aging is but one element of clinical aging, however, others being heredity and environment. Although telomerase expression is an important marker of malignancy, it is not itself the cause of cancer. Telomerase expression and telomere lengthening apparently do not alter normal cell cycle control, chromosome complement, or cell morphology.