Medical researchers are learning a great deal about the age-related degeneration of human biochemistry by looking at the extreme edge cases and malfunctions - such as Li-Fraumeni syndrome in the case of increased cancer risk with advancing age: "Li-Fraumeni was associated with inheritance of a mutated form of the p53 tumor suppressor gene, but we also noticed each generation developed cancer earlier than the preceding generation ... we have discovered that telomeres become shorter in each generation of disease carriers, leading to a genetic instability that primes them for progressively earlier cancers ... Telomeres are repeated sequences of DNA at the tips of every chromosome that function as a sort of genetic slack. As cells grow and divide throughout life, the chromosomes, which contain all of an individual's genetic information, replicate as well. The enzymes that create copies of chromosomes cannot, however, physically reach the very end of the chromosome, so they leave a minute bit of this telomere slack behind each time. This is known to researchers as the 'end replication problem' and has made telomeres an important subject of research in the science of aging and cancer." What then is the mechanism linking p53 and telomere length?

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2007-02/aafc-scc021507.php
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