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JNCI Journal of the National Cancer Institute 2003 95(13):926-927; doi:10.1093/jnci/95.13.926
© 2003 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 95, No. 13, 926-927, July 2, 2003
© 2003 Oxford University Press

EDITORIAL

New Leads Suggest a Clinically Relevant Genotype–Phenotype Relationship for the p53 Gene

Frederic J. Kaye, Takefumi Komiya

Affiliation of authors: Genetics Branch, Center for Cancer Research, National Cancer Institute and the National Naval Medical Center, Bethesda, MD.

Correspondence to: Frederic J. Kaye, M.D., Genetics Branch, Center for Cancer Research, National Cancer Institute and the National Naval Medical Center, Bldg. 8, Rm. 5101, Bethesda, MD 20889 (e-mail: kayef@navmed.nci.nih.gov).

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The literature dedicated to the functional properties of the p53 gene can make one wish that there were more genes in the human genome and far fewer functions for each protein product. p53, arguably the most heavily studied gene product, can interact with a wide array of nuclear and cytoplasmic binding partners. These interactions, as well as subtle posttranslational changes in phosphorylation, acetylation, sumoylation, and other modifications, can modulate the central activity of p53—the transcriptional activation (and occasional repression) of downstream target genes. Although there is increasing evidence for unexpected nontranscriptional roles for p53 (1), the regulation of target gene expression in concert with individual components of parallel and interconnecting cell signaling cascade pathways mediates the primary function of p53, which has been reviewed extensively (2). This function can be summarized as the ability to sense and respond to cellular stresses that can range from dramatic . . . [Full Text of this Article]


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