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Journal of the National Cancer Institute Advance Access originally published online on May 27, 2008
JNCI Journal of the National Cancer Institute 2008 100(11):757-759; doi:10.1093/jnci/djn156
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© The Author 2008. Published by Oxford University Press.

EDITORIALS

Tumor Suppression for ARFicionados: The Relative Contributions of p16INK4a and p14ARF in Melanoma

Gordon Peters

Affiliation of author: Cancer Research UK London Research Institute, London, UK

Correspondence to: Gordon Peters, PhD, Cancer Research UK London Research Institute, 44 Lincoln’s Inn Fields, London WC2A 3PX, UK (e-mail: gordon.peters@cancer.org.uk).

The first 150 words of the full text of this article appear below.

Glancing at the title of the article by Freedberg et al. (1), readers might wonder why almost 15 years after the connection between p16INK4a and melanoma was first reported, people still seem to be questioning its importance. The confounding factor is that the gene is embedded in a locus that encodes not one but three potential tumor suppressors, INK4a, INK4b, and ARF, each vying for a share of the limelight. The two INK4 proteins, p15INK4b and p16INK4a, are cyclin-dependent kinase (CDK) inhibitors that activate the retinoblastoma (pRb) pathway, whereas p14ARF, which exploits the second exon of p16INK4a in an alternative reading frame, is an activator of p53. Elevated expression of any one of these proteins causes cell cycle arrest, but the main arena in which their effects are manifest is the implementation of cellular senescence, the state of irreversible growth arrest elicited by various forms of . . . [Full Text of this Article]


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