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Nevus Senescence
Joint Authors
Sanchez, Margaret I.
Grichnik, James M.
Ross, Andrew L.
Source
Issue
Vol. 2011, Issue 2011 (31 Dec. 2011), pp.1-8, 8 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2011-06-22
Country of Publication
Egypt
No. of Pages
8
Main Subjects
Abstract EN
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.
American Psychological Association (APA)
Ross, Andrew L.& Sanchez, Margaret I.& Grichnik, James M.. 2011. Nevus Senescence. ISRN Dermatology،Vol. 2011, no. 2011, pp.1-8.
https://search.emarefa.net/detail/BIM-487577
Modern Language Association (MLA)
Ross, Andrew L.…[et al.]. Nevus Senescence. ISRN Dermatology No. 2011 (2011), pp.1-8.
https://search.emarefa.net/detail/BIM-487577
American Medical Association (AMA)
Ross, Andrew L.& Sanchez, Margaret I.& Grichnik, James M.. Nevus Senescence. ISRN Dermatology. 2011. Vol. 2011, no. 2011, pp.1-8.
https://search.emarefa.net/detail/BIM-487577
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-487577