Telomeres And Telomerase (page 2/3) | ||
As we age, our levels of telomerase decline. This means that there is less telomerase directing the relengthening process, which then leads to the consequences we have just looked at: telomeres growing shorter, cells reaching the Hayflick limit and becoming senescent, impending organ failure, and eventual death. The trick, then, is to step in somewhere along the causal chain and prevent the telomeres from growing shorter. Some of the research going on today is looking into the regulatory effects that hormones may bring to bear on telomerase production. One study, involving the use of testosterone on stem cells of the rat prostate, has demonstrated that such regulation is possible. Other studies have been looking into the regulatory effects of estrogen on human endometrial cells. These studies, as well, show that regulation of telomerase activity by hormonal means is possible. Another hormone, epidermal growth factor, has shown a strong effect in producing telomerase activity in human epidermal cells. HGH is also thought to hold strong promise in promoting the release of life-lengthening telomerase.
Trials of human telomerase therapy are close to starting at this time for conditions such as cirrhosis of the liver.
Dr. Robert Weinberg of MIT's Whitehead Institute says: Most cancer cells produce telomerase to allow themselves to grow forever if nutrition is available. Stopping telomerase production kills the cancer cells. Agents that stop telomerase may be universal chemotherapeutic agents for all tumor types. At this time scientists at Geron Corporation in San Francisco have developed assays to detect telomerase activity and therefore detect cancer. Also, cytotoxic T-cells may be programmed by vaccination to destroy cancer cells that produce excess telomerase. Adenoviruses at this time are also being programmed to enter telomerase producing cancer cells and activate thymidine kinase suicide gene. But how will this help with longevity? | ||
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