Cellular Senescence: Many Roads, One Final Destination

Cellular senescence is a tumor-suppressor mechanism that has been shown to occur in response to multiple signals, including oncogenic stress, DNA damage, oxidative stress, telomere shortening, and other tumor-promoting insults. Over the past decade, much has been uncovered regarding the phenotype of...

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Main Author: Raya Saab
Format: Article
Language:English
Published: Wiley 2010-01-01
Series:The Scientific World Journal
Online Access:http://dx.doi.org/10.1100/tsw.2010.68
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author Raya Saab
author_facet Raya Saab
author_sort Raya Saab
collection DOAJ
description Cellular senescence is a tumor-suppressor mechanism that has been shown to occur in response to multiple signals, including oncogenic stress, DNA damage, oxidative stress, telomere shortening, and other tumor-promoting insults. Over the past decade, much has been uncovered regarding the phenotype of this tumor-suppressor response and the underlying pathways necessary for its establishment. However, we have also learned that the intricate details of signaling pathways underlying senescence as a tumor-suppressor response are very much context dependent. In addition, cross-talk among pathways, and negative and positive feedback loops, all complicate our understanding of this process. This short review attempts to summarize what is known to date regarding senescence in tumor suppression, both in vitro and in vivo. Further insights into pathways necessary for senescence will hopefully identify appropriate targets for interventions to not only induce senescence as a treatment of cancerous lesions, but also to maintain this state in premalignant lesions in an effort to prevent progression to cancer.
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spelling doaj-art-7f2099f7fea349c1918b7b85e24be9fa2025-08-20T02:08:43ZengWileyThe Scientific World Journal1537-744X2010-01-011072774110.1100/tsw.2010.68Cellular Senescence: Many Roads, One Final DestinationRaya Saab0Children's Cancer Center of Lebanon, American University of Beirut, LebanonCellular senescence is a tumor-suppressor mechanism that has been shown to occur in response to multiple signals, including oncogenic stress, DNA damage, oxidative stress, telomere shortening, and other tumor-promoting insults. Over the past decade, much has been uncovered regarding the phenotype of this tumor-suppressor response and the underlying pathways necessary for its establishment. However, we have also learned that the intricate details of signaling pathways underlying senescence as a tumor-suppressor response are very much context dependent. In addition, cross-talk among pathways, and negative and positive feedback loops, all complicate our understanding of this process. This short review attempts to summarize what is known to date regarding senescence in tumor suppression, both in vitro and in vivo. Further insights into pathways necessary for senescence will hopefully identify appropriate targets for interventions to not only induce senescence as a treatment of cancerous lesions, but also to maintain this state in premalignant lesions in an effort to prevent progression to cancer.http://dx.doi.org/10.1100/tsw.2010.68
spellingShingle Raya Saab
Cellular Senescence: Many Roads, One Final Destination
The Scientific World Journal
title Cellular Senescence: Many Roads, One Final Destination
title_full Cellular Senescence: Many Roads, One Final Destination
title_fullStr Cellular Senescence: Many Roads, One Final Destination
title_full_unstemmed Cellular Senescence: Many Roads, One Final Destination
title_short Cellular Senescence: Many Roads, One Final Destination
title_sort cellular senescence many roads one final destination
url http://dx.doi.org/10.1100/tsw.2010.68
work_keys_str_mv AT rayasaab cellularsenescencemanyroadsonefinaldestination