An interventional study of Erbium:YAG and UV endonuclease from Micrococcus luteus in p53 Expression, sponsored by Moy-Fincher-Chipps Facial Plastics and Dermatology. Status unknown. Open to participants aged 18 Years and older, including healthy volunteers. Per ClinicalTrials.gov, last updated 2020-02-20.
Sponsored by Moy-Fincher-Chipps Facial Plastics and Dermatology · Not applicable, Interventional, and Treatment
The p53 gene is located on the short arm of chromosome 17 and serves as a tumor suppressor gene. Alteration in p53 is an early event in skin cancer development. Further, p53 is the most commonly mutated gene in non-melanocytic skin cancers. The presence of p53 within epidermal skin cells is believed to reflect the malignant potential of photo-damaged skin. Studies have demonstrated that increasing sun exposure and age are directly associated with higher levels of p53 in facial skin. Consequently, the physiologic overexpression of p53 present in epidermal skin may be indicative of both past photodamage and future risk for developing skin cancer. Advancements in dermatologic research have allowed clinicians to treat photo-damaged skin with with novel modalities. For example, epidermal ablation with the 2,940nm fractional erbium laser has been shown to reduce the risk of carcinogenesis by promoting apoptosis, working similarly to p53. Laser resurfacing results in the replacement of epidermal cells once the necrotic debris is cleared away. This therapeutic effect of laser resurfacing may be gauged by cutaneous p53 expression before and after such interventions. Investigators have noted the reliability of cutaneous p53 expression to gauge therapeutic effects in patients receiving erbium doped yttrium aluminum garnet laser (Er:YAG), dermabrasion, and CO2 laser. Similarly to laser resurfacing, topical DNA repair enzymes have been shown to be protective against skin cancer development and, therefore, may also reduce epidermal p53 expression. UV endonuclease, a DNA repair enzyme derived from the UV-resistant microbe Micrococcus luteus, enhances DNA repair by removing cyclobutane pyrimidine dimers (CPDs) induced by ultraviolet radiation (UVR). To efficiently penetrate the stratum corneum, this enzyme is encapsulated within liposomes, which facilitate entry into keratinocyte nuclei. Once exposed to CPDs, UV endonuclease repairs DNA by catalyzing two reactions: the first uses glycosylase, which releases thymine and causes an apurinic site; the second involves lyase, which incises the phosphodiester backbone, causing a single stranded break. An exonuclease then removes bases around this site, and a polymerase fills the gap, thereby repairing the photodamaged DNA. In addition to repairing damaged DNA on the molecular level, UV endonuclease has also demonstrated the ability to clinically decrease non-melanocytic skin cancer and pre-cancer development. The capability of topical DNA repair enzymes to reverse DNA damage leads us to believe that it will also lead to a reduction in p53 expression within epidermal cells. For these reasons, we wish to investigate the role of 2,940 fractional erbium laser and topical DNA repair enzymes on reducing cutaneous p53 expression.
This is the only study on the registry with Moy-Fincher-Chipps Facial Plastics and Dermatology as lead sponsor.
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Exclusion Criteria:
All participants will receive Erbium laser treatment on their right post-auricular region
Device: Erbium:YAG
All participants will apply topical DNA repair enzymes on their left post-auricular region
Drug: UV endonuclease from Micrococcus luteus
Treatment with Erbium:YAG laser
Application of topical DNA repair enzymes
p53 expression
p53 epidermal expression will be evaluated by scoring the nuclear staining of basilar cells in 3-mm punch biopsies, knowing that the basal layer gives rise to dysplasia. The numbers of stained cells present at the 3-month visit will be compared with the number of stained cells present at the baseline visit.
Time frame: 3 months
No study locations are listed for this record.
Plan to share: No — We are currently in the process of determine the IPD sharing plan
Start is estimated for Apr 2020; primary completion for Jun 2020, 2 months later.
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This study is status unknown, as verified in Feb 2020. You cannot join it, but the record below documents what was studied.
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