Table of Contents
ISRN Dermatology
Volume 2011, Article ID 642157, 8 pages
Research Article

Nevus Senescence

1Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL 33136, USA
2Melanoma Program, Sylvester Comprehensive Cancer Center, Miller School of Medicine, University of Miami, Miami, FL 33136, USA
3Interdisciplinary Stem Cell Institute, Miller School of Medicine, University of Miami, Miami, FL 33136, USA

Received 4 April 2011; Accepted 30 April 2011

Academic Editors: M. Alaibac, S.-C. Chao, and N. Darwiche

Copyright © 2011 Andrew L. Ross et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Melanomas and nevi share many of the same growth-promoting mutations. However, melanomas grow relentlessly while benign nevi eventually undergo growth arrest and stabilize. The difference in their long-term growth potential may 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.