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Wounding Therapies for Prevention of Photocarcinogenesis
The occurrence of non-melanoma skin cancer (NMSC) is closely linked with advanced age and ultraviolet-B (UVB) exposure. More specifically, the development of NMSC is linked to diminished insulin-like growth factor-1 (IGF-1) signaling from senescent dermal fibroblasts in geriatric skin. Consequently,...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8776632/ https://www.ncbi.nlm.nih.gov/pubmed/35071017 http://dx.doi.org/10.3389/fonc.2021.813132 |
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author | Frommeyer, Timothy C. Rohan, Craig A. Spandau, Dan F. Kemp, Michael G. Wanner, Molly A. Tanzi, Elizabeth Travers, Jeffrey B. |
author_facet | Frommeyer, Timothy C. Rohan, Craig A. Spandau, Dan F. Kemp, Michael G. Wanner, Molly A. Tanzi, Elizabeth Travers, Jeffrey B. |
author_sort | Frommeyer, Timothy C. |
collection | PubMed |
description | The occurrence of non-melanoma skin cancer (NMSC) is closely linked with advanced age and ultraviolet-B (UVB) exposure. More specifically, the development of NMSC is linked to diminished insulin-like growth factor-1 (IGF-1) signaling from senescent dermal fibroblasts in geriatric skin. Consequently, keratinocyte IGF-1 receptor (IGF-1R) remains inactive, resulting in failure to induce appropriate protective responses including DNA repair and cell cycle checkpoint signaling. This allows UVB-induced DNA damage to proliferate unchecked, which increases the likelihood of malignant transformation. NMSC is estimated to occur in 3.3 million individuals annually. The rising incidence results in increased morbidity and significant healthcare costs, which necessitate identification of effective treatment modalities. In this review, we highlight the pathogenesis of NMSC and discuss the potential of novel preventative therapies. In particular, wounding therapies such as dermabrasion, microneedling, chemical peeling, and fractionated laser resurfacing have been shown to restore IGF-1/IGF-1R signaling in geriatric skin and suppress the propagation of UVB-damaged keratinocytes. This wounding response effectively rejuvenates geriatric skin and decreases the incidence of age-associated NMSC. |
format | Online Article Text |
id | pubmed-8776632 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-87766322022-01-22 Wounding Therapies for Prevention of Photocarcinogenesis Frommeyer, Timothy C. Rohan, Craig A. Spandau, Dan F. Kemp, Michael G. Wanner, Molly A. Tanzi, Elizabeth Travers, Jeffrey B. Front Oncol Oncology The occurrence of non-melanoma skin cancer (NMSC) is closely linked with advanced age and ultraviolet-B (UVB) exposure. More specifically, the development of NMSC is linked to diminished insulin-like growth factor-1 (IGF-1) signaling from senescent dermal fibroblasts in geriatric skin. Consequently, keratinocyte IGF-1 receptor (IGF-1R) remains inactive, resulting in failure to induce appropriate protective responses including DNA repair and cell cycle checkpoint signaling. This allows UVB-induced DNA damage to proliferate unchecked, which increases the likelihood of malignant transformation. NMSC is estimated to occur in 3.3 million individuals annually. The rising incidence results in increased morbidity and significant healthcare costs, which necessitate identification of effective treatment modalities. In this review, we highlight the pathogenesis of NMSC and discuss the potential of novel preventative therapies. In particular, wounding therapies such as dermabrasion, microneedling, chemical peeling, and fractionated laser resurfacing have been shown to restore IGF-1/IGF-1R signaling in geriatric skin and suppress the propagation of UVB-damaged keratinocytes. This wounding response effectively rejuvenates geriatric skin and decreases the incidence of age-associated NMSC. Frontiers Media S.A. 2022-01-07 /pmc/articles/PMC8776632/ /pubmed/35071017 http://dx.doi.org/10.3389/fonc.2021.813132 Text en Copyright © 2022 Frommeyer, Rohan, Spandau, Kemp, Wanner, Tanzi and Travers https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Oncology Frommeyer, Timothy C. Rohan, Craig A. Spandau, Dan F. Kemp, Michael G. Wanner, Molly A. Tanzi, Elizabeth Travers, Jeffrey B. Wounding Therapies for Prevention of Photocarcinogenesis |
title | Wounding Therapies for Prevention of Photocarcinogenesis |
title_full | Wounding Therapies for Prevention of Photocarcinogenesis |
title_fullStr | Wounding Therapies for Prevention of Photocarcinogenesis |
title_full_unstemmed | Wounding Therapies for Prevention of Photocarcinogenesis |
title_short | Wounding Therapies for Prevention of Photocarcinogenesis |
title_sort | wounding therapies for prevention of photocarcinogenesis |
topic | Oncology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8776632/ https://www.ncbi.nlm.nih.gov/pubmed/35071017 http://dx.doi.org/10.3389/fonc.2021.813132 |
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