Anna Liachenko, BSc, MSc
Managing Editor,
Geriatrics & Aging
The relationship between aging and cancer has its basis in cell cycle alterations. While multiple factors affect cell cycle progression, recent research has directed a great deal of attention to telomere length as a key factor affecting mammalian cell proliferation. This article discusses recent findings with respect to the role of telomeres and telomerase in cancer, cellular aging, and longevity.
Telomeres are short DNA repeats located at the ends of eukaryotic chromosomes. Telomeres cap chromosomal ends preventing the loss of important genes during cell division. With every cell division, the length of telomeres decreases unless it is corrected by telomerase, a ribonucleoprotein enzyme that extends the telomeres by adding hexameric nucleotide repeats to the ends of chromosomes. In humans, telomeres are short, and telomerase activity is low in many somatic tissues but is present in germ cells, activated leukocytes, and stem cells from a variety of organs. The study of telomeres has been hampered by the fact that classical animal models, such as mice, have highly active telomerase. This results in long telomeres that do not shorten enough during the animal lifespan to play a significant role in cellular aging. Recently, a genetically altered telomerase-deficient mouse model has been created by a group of researchers at Harvard.
