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JNCI Journal of the National Cancer Institute 2001 93(2):82-83; doi:10.1093/jnci/93.2.82
© 2001 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 93, No. 2, 82-83, January 17, 2001
© 2001 Oxford University Press

EDITORIAL

Individual Variation in p53 Responsiveness

Mats Ljungman

Correspondence to: Mats Ljungman, Ph.D., Department of Radiation Oncology, Division of Cancer Biology, University of Michigan Comprehensive Cancer Center, Program in Cellular and Molecular Biology, University of Michigan Medical School, 4306 CCGC, 1500 E. Medical Center Dr., Ann Arbor, MI 48109–0936 (e-mail: ljungman@umich.edu).

The tumor suppressor p53 is part of the cellular emergency team that is designated to respond to various cellular stresses such as DNA damage. After exposure to UV or ionizing radiation, p53 proteins accumulate in the nucleus and transactivate specific target genes. Expression of the p53-inducible p21WAF1 gene product enhances the survival of cells by activating cell cycle checkpoints, thus allowing the cell to have more time for DNA repair before entering S phase or mitosis. However, p53 can also stimulate cells to undergo apoptosis, a programmed cell death pathway. These activities of p53 contribute to the protection of the organism from acquiring mutated cells . . . [Full Text of this Article]

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