Nevus senescence: An update

Andrew L. Ross, Margaret I. Sanchez, James M Grichnik

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Nevi and melanomas share the many of the same growth-promoting mutations. However, benign nevi eventually undergo growth arrest and stabilize while melanomas grow relentlessly. The difference in their long-term growth potential can in part be attributed to activation of cellular senescence pathways. The primary mediator of senescence in nevi appears to be p16. Redundant, secondary senescence systems are also present and include the p14-p53-p21 pathway, the IGFBP7 pathway, the FBXO31 pathway, and the PI3K-mediated stress-induced endoplasmic reticulum unfolded protein response. It is evident that these senescence pathways result in an irreversible arrest in most instances; however, they can clearly be overcome in melanoma. Circumvention of these pathways is most frequently associated with gene deletion or transcriptional repression. Reactivation of senescence mechanisms could serve to inhibit melanoma tumor progression.

Original languageEnglish (US)
Title of host publicationNevogenesis: Mechanisms and Clinical Implications of Nevus Development
PublisherSpringer Berlin Heidelberg
Pages117-126
Number of pages10
ISBN (Print)9783642283970, 9783642283963
DOIs
StatePublished - Jan 1 2012

ASJC Scopus subject areas

  • Medicine(all)

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    Ross, A. L., Sanchez, M. I., & Grichnik, J. M. (2012). Nevus senescence: An update. In Nevogenesis: Mechanisms and Clinical Implications of Nevus Development (pp. 117-126). Springer Berlin Heidelberg. https://doi.org/10.1007/978-3-642-28397-0_10