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Nevogenesis pp 117-126 | Cite as

Nevus Senescence: An Update

  • Andrew L. Ross
  • Margaret I. Sanchez
  • James M. GrichnikEmail author
Chapter
  • 466 Downloads

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.

Keywords

Unfold Protein Response Senescent Cell Primary Mediator BRAFV600E Mutation Molecular Mediator 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

Conflict of Interest

DigitalDerm, Inc – major shareholder. Spectral Image, Inc – past grants and consulting. MELA Sciences – past grants and consulting. Genentech – ­consultant. Archives of Dermatology, skINsight – section editor.

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Copyright information

© Springer- Verlag Berlin Heidelberg 2012

Authors and Affiliations

  • Andrew L. Ross
    • 1
  • Margaret I. Sanchez
    • 1
  • James M. Grichnik
    • 1
    • 2
    • 3
    Email author
  1. 1.Department of Dermatology and Cutaneous SurgeryUniversity of Miami Miller School of MedicineMiamiUSA
  2. 2.Melanoma Program, Department of Dermatology and Cutaneous SurgerySylvester Comprehensive Cancer CenterMiamiUSA
  3. 3.Interdisciplinary Stem Cell Institute, Miller School of MedicineUniversity of MiamiMiamiUSA

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