Nevus senescence.

ISRN Dermatology
Andrew L RossJames M Grichnik

Abstract

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.

References

Mar 1, 1991·Mutation Research·C B Harley
Jan 1, 1989·Genome Génome / Conseil National De Recherches Canada·E H BlackburnD Shippen-Lentz
Sep 26, 1995·Proceedings of the National Academy of Sciences of the United States of America·G P DimriO Pereira-Smith
Jan 1, 1996·Journal of Cancer Research and Clinical Oncology·T PappD Schiffmann
May 1, 1996·Biological Signals·G P DimriJ Campisi
Oct 31, 1997·Journal of the American Academy of Dermatology·R A ZeffJ M Grant-Kels
Nov 14, 1997·Genes & Development·L ChinR A DePinho
Jul 3, 1998·The American Journal of Dermatopathology·L E SparrowP J Heenan
Sep 3, 1998·The Journal of Biological Chemistry·J YanJ F Hancock
Jun 15, 1994·Physical Review. B, Condensed Matter·L DouillardG Tourillon
Apr 18, 2000·Journal of the American Academy of Dermatology·H J LeeJ W Kim
Aug 15, 2000·Annual Review of Nutrition·S J FomonE E Ziegler
Apr 19, 2002·Carcinogenesis·Dania Alarcon-Vargas, Ze'ev Ronai
Jun 29, 2002·Nature Biotechnology·Woodring E Wright, Jerry W Shay
Jul 9, 2002·Pigment Cell Research·Dorothy C Bennett, Estela E Medrano
Aug 13, 2003·The EMBO Journal·Christian M BeauséjourJudith Campisi
Aug 16, 2003·Dermatology : International Journal for Clinical and Investigative Dermatology·Toshiro KageshitaTomomichi Ono
Aug 12, 2004·The Journal of Investigative Dermatology·Scott R FlorellSancy A Leachman
Oct 9, 2004·Carcinogenesis·Jerry W Shay, Woodring E Wright
Dec 22, 2004·Mechanisms of Ageing and Development·T von ZglinickiS P Jackson
Dec 29, 2004·Current Biology : CB·Jacqueline J L Jacobs, Titia de Lange
Aug 5, 2005·Nature·Chrysiis MichaloglouDaniel S Peeper
Sep 17, 2005·Genes & Development·Titia de Lange
Dec 16, 2005·The Journal of Investigative Dermatology·Scott R FlorellSancy A Leachman
Jan 19, 2006·The Journal of Investigative Dermatology·Pablo UribeSergio Gonzalez
May 26, 2006·Nature Reviews. Cancer·Manuel Collado, Manuel Serrano
Sep 22, 2006·Antioxidants & Redox Signaling·Toren Finkel
Oct 19, 2006·Cancer Research·Alisa M GoldsteinUNKNOWN Melanoma Genetics Consortium (GenoMEL)
Oct 24, 2006·Cell·William Y Kim, Norman E Sharpless
Dec 1, 2006·Nature·Raffaella Di MiccoFabrizio d'Adda di Fagagna
Jan 11, 2007·Genes & Development·Frédérick A MalletteGerardo Ferbeyre

❮ Previous
Next ❯

Citations

Mar 20, 2015·Molecular Carcinogenesis·Tahseen H NastiCraig A Elmets
Sep 24, 2015·Cancers·Chandra Prakash PrasadTommy Andersson
Dec 1, 2011·Chemistry : a European Journal·Ulyana ShimanovichAharon Gedanken

❮ Previous
Next ❯

Related Concepts

Related Feeds

AKT Pathway

This feed focuses on the AKT serine/threonine kinase, which is an important signaling pathway involved in processes such as glucose metabolism and cell survival.

© 2022 Meta ULC. All rights reserved