Chromosomes, which store our genetic iformation in the form of DNA, are vulnerable to damage by 'fraying' at their ends. Here, special protective structures called telomeres are continually repaired by the enzyme telomerase, preventing the loss of important information. As our cells age, however, it is thought that a gradual erosion of telomere DNA is linked to an increased incidence of cancer.
In Nature [Vol. 406, Issue 6796 (2000), p. 641], Ronald DePinho of Harvard Medical School, Boston, USA, and colleagues, report the generation of mice which lack telomerase and p53, another protein which is responsible for protecting genetic information. Intriguingly, the mutant mice develop cancers which are typical of those seen in ageing humans, including breast and colon carcinomas. Looking directly at the chromosomes of the mutant mice reveals frequent 'non-reciprocal translocations', in which DNA from one chromosome is joined incorrectly and irreversibly to the end of another chromosome, another hallmark of human cancer.
These studies should help us to understand the mechanisms underlying the development of common human cancers. Could telomerase be a target for new anticancer drug therapies? Discussing the research in an accompanying News & Views article (p. 573), Douglas Hanahan of the University of California at San Francisco advises caution.
Ronald DePinho tel +1 617 632 6085,
fax +1 617 632 6069,
Douglas Hanahan tel +1 415 476 9209,
fax +1 415 731 3612,
(C) Nature press release
Message posted by: Trevor M. D'Souza
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