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Extending telomeres can allow cells to divide more and increase the risk of uncontrolled cell growth and cancer development. [24] A study conducted by Johns Hopkins University challenged the idea that long telomeres prevent aging. Rather than protecting cells from aging, long telomeres help cells with age-related mutations last longer. [13]
Telomere shortening is associated with aging, mortality, and aging-related diseases in experimental animals. [ 8 ] [ 34 ] Although many factors can affect human lifespan, such as smoking, diet, and exercise, as persons approach the upper limit of human life expectancy , longer telomeres may be associated with lifespan.
A non-programmed theory of mammal ageing [38] states that different species possess different capabilities for maintenance and repair. Longer-lived species possess many mechanisms for offsetting damage due to causes such as oxidation, telomere shortening, and other deteriorative processes.
The successive shortening of the chromosomal telomeres with each cell cycle is also believed to limit the number of divisions of the cell, contributing to aging. After sufficient shortening, proteins responsible for maintaining telomere structure, such as TRF2, are displaced, resulting in the telomere being recognized as a site of a double ...
The role of telomeres and telomerase in cell aging and cancer was established by scientists at biotechnology company Geron with the cloning of the RNA and catalytic components of human telomerase [9] and the development of a polymerase chain reaction (PCR) based assay for telomerase activity called the TRAP assay, which surveys telomerase ...
Alexey Matveyevich Olovnikov (Russian: Алексей Матвеевич Оловников; 10 October 1936 – 6 December 2022) was a Russian biologist.Among other things, in 1971, he was the first to recognize the problem of telomere shortening, to predict the existence of telomerase, and to suggest the telomere hypothesis of aging and the relationship of telomeres to cancer.
Resolving the question of why cancer cells have short telomeres led to the development of a two-stage model for how cancer cells subvert telomeric regulation of the cell cycle. First, the DNA damage checkpoint must be inactivated to allow cells to continue dividing even when telomeres pass the critical length threshold.
Normal aging is associated with telomere shortening in both humans and mice, and studies on genetically modified animal models suggest causal links between telomere erosion and aging. [10] Leonard Hayflick demonstrated that a normal human fetal cell population will divide between 40 and 60 times in cell culture before entering a senescence phase.