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Published on: October 25, 2018
How Wounding via Lasers Has Potential Photocarcinogenic Preventative Effects via Dermal Remodeling
Aleksandar Krbanjevic1, Jeffrey B Travers2, Dan F Spandau3
1Department of Dermatology, Indiana University School of Medicine, 975 West Walnut Street, Rm 349, Indianapolis, IN 46202, 317-274-7115.
Abstract:
As the incidence of non-melanoma skin cancer (NMSC) is increasing, there is a growing need to identify effective preventive strategies. A recently proposed hypothesis states that NMSC photocarcinogenesis is tightly linked to insufficient insulin growth factor-1 expression by agglomerated senescent fibroblasts in geriatric dermis. This paucity of IGF-1 expression in senile skin allows basal keratinocytes to mitotically propagate their UVB-altered genome and potentially initiate an actinic neoplasm. Here we review the role of the dermal microenvironment in NMSC pathogenesis, describe the impact of fibroblast senescence on this process and discuss how laser-induced dermal wounding can be effectively used to prevent NMSC development in geriatric patients.
Insights
Non-melanoma skin cancer (NMSC) may be prevented by addressing fibroblast senescence in aging skin. Laser treatments may improve insulin growth factor-1 (IGF-1) expression, reducing NMSC risk.
Area of Science:
- Dermatology
- Oncology
- Gerontology
Background:
- Non-melanoma skin cancer (NMSC) incidence is rising globally.
- Aging skin presents unique challenges for cancer prevention.
- Fibroblast senescence in the dermal microenvironment is implicated in NMSC pathogenesis.
Purpose of the Study:
- To review the role of the dermal microenvironment in NMSC.
- To describe the impact of fibroblast senescence on NMSC development.
- To discuss laser-induced dermal wounding as a preventive strategy for NMSC in geriatric patients.
Main Methods:
- Literature review on NMSC photocarcinogenesis.
- Analysis of the role of fibroblast senescence and insulin growth factor-1 (IGF-1) in aging skin.
- Exploration of laser-induced dermal wounding as a potential NMSC preventive measure.
Main Results:
- Insufficient IGF-1 expression by senescent fibroblasts in geriatric dermis is linked to NMSC.
- Senescent fibroblasts allow UVB-damaged keratinocytes to proliferate, potentially initiating actinic neoplasms.
- Laser-induced dermal wounding may counteract these effects.
Conclusions:
- The dermal microenvironment, particularly fibroblast senescence, plays a critical role in NMSC development.
- Restoring IGF-1 expression or mitigating senescence may offer preventive strategies.
- Laser therapy presents a promising avenue for NMSC prevention in the elderly population.
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