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Previous Volume 332:955-956 April 6, 1995 Number 14 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Numerous genetic accidents, including the activation of proto-oncogenes and the loss of tumor-suppressor genes, can result in the stimulation of cell division. However, mammalian cells have evolved an intricate set of checks and balances against uncontrolled cellular proliferation. One of these is cellular suicide, or apoptosis, triggered by the p53 gene in the presence of aberrant growth signals. Another appears to be the progressive shortening of the ends of chromosomes, or telomeres, that accompanies normal cell division and may contribute to cellular aging. Support for this concept comes from a recent article in Science by Kim and coworkers,¹ reporting a . . . [Full Text of this Article]

References

This article has been cited by other articles:

• Belair, C. D., Yeager, T. R., Lopez, P. M., Reznikoff, C. A. (1997). Telomerase activity: A biomarker of cell proliferation, not malignant transformation. Proc. Natl. Acad. Sci. USA 94: 13677-13682 [Abstract] [Full Text]