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In 1961 Dr. Leonard Hayflick published a paper showing that human cells grown in a petri dish do not divide indefinitely like most bacteria and other single cellular organisms do [2]. Dr. Hayflick had essentially discovered “senescence”. This has since been repeated by 1000’s of other labs and confirmed to be real. Dr. Hayflick and many others were also able to show that cells obtained from a young person could divide more times before reaching senescence then cells from an old person. This limit to the number of times a human cell could divide became known as the “Hayflick Limit”. For at least the next 35 years no one knew what caused senescence and it was considered as a feature of mammalian cells that was impossible to prevent. But, in 1998 Dr. Andrews and his team showed that senescence could be prevented by preventing telomere shortening [3].
Telomeres were first discovered by Hermann Muller in 1938 and Barbara McClintock in 1940 [4, 5]. The discovery of how to prevent senescence by lengthening telomeres began with the publication of the paper entitled “The Telomere Hypothesis of Aging” by Dr. Calvin Harley and Dr. Richard Allsopp [6]. Prior to that publication no other theory to explain aging made sense. A theory has to explain everything about aging not just some of the things. If it can’t explain everything than the theory is flawed or incomplete. Key problems with all other theories are that they couldn’t explain why people that lived near the North and South Poles aged at the same rate as people that lived near the equator. All those theories also couldn’t explain why Dogs and Cats age at entirely different rates than humans. But the Telomere Theory of Aging explained everything.
Frustrated from over 30 years of being unable to logically or statistically justify any of the other theories about aging, Dr. Andrews found himself almost instantly working with Drs. Harley and Allsopp at Geron Corporation to test their hypothesis after reading their paper. Dr. Andrews had concluded years earlier that the only way to explain everything about aging was to propose the existence of a ticking clock in human cells. He envisioned that human cells must have something equivalent to “ride tickets at an amusement park” that get used up one at a time each time a human cell divides. Telomere shortening was the first thing, and still only thing, that Dr. Andrews ever learned of that could be equivalent to the ride tickets. In order to test Harley’s and Allsopp’s hypothesis, Dr. Andrews first had to discover an enzyme called Human Telomerase that Harley and Allsopp proposed to exist in human cells that could lengthen telomeres. Labs all over the world spent years painstakingly searching for the existence of human telomerase with no success. Dr. Andrews began working with Harley and Allsopp in December of 1993 and his team discovered the gene for the “human Telomerase RNA” (hTR) component of human telomerase, on the “q” arm of Chromosome 3, within three months in early April of 1994.
The paper was published in 1995 [7]. Shortly, thereafter, his team discovered the RNA component of telomerase in other animals including mice (mTR), canines (cTR), felines (fTR), and etc. He also found that none of the mammalian RNA components showed any sequence resemblance to the RNA component previously discovered in tetrahymena [8] nine years earlier. Dr. Andrews’ team was able to show that hTR was not the key to why most cells have telomere shortening because hTR was present even in cells that experienced telomere shortening [7]. It was ubiquitous in all human cells. Nevertheless, Dr. Andrews’ team was able to show that the anti-sense of hTR inhibits telomere lengthening and kills almost all cancer cells, by forcing their telomeres to shorten, and causing the cancers to die from aging, without having any effect on non-cancer cells [7]. This not only proved that hTR was essential for telomerase function, but its inhibition was hailed as one of the greatest discoveries ever towards possibly curing cancer.
