To Evaluate and Compare p53 Epidermal Expression in Healthy Volunteers 3 Months After Treatment With a 2,940-nm Fractional Ablative Erbium Laser and Topical DNA Repair Enzymes

NCT ID: NCT04277949

Last Updated: 2020-02-20

Basic Information

• Recruitment Status: UNKNOWN
• Clinical Phase: NA
• Total Enrollment: 10 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2020-04-30
• Study Completion Date: 2020-08-31

Brief Summary

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.

Conditions

p53 Expression

Study Design

• Allocation Method: NON_RANDOMIZED
• Intervention Model: SINGLE_GROUP
• Primary Study Purpose: TREATMENT
• Blinding Strategy: NONE

Study Groups

Erbium laser

All participants will receive Erbium laser treatment on their right post-auricular region

Group Type: EXPERIMENTAL

Erbium:YAG

Intervention Type: DEVICE

Treatment with Erbium:YAG laser

DNA repair enzyme

All participants will apply topical DNA repair enzymes on their left post-auricular region

Group Type: EXPERIMENTAL

UV endonuclease from Micrococcus luteus

Intervention Type: DRUG

Application of topical DNA repair enzymes

Interventions

Erbium:YAG

Treatment with Erbium:YAG laser

Intervention Type: DEVICE

UV endonuclease from Micrococcus luteus

Application of topical DNA repair enzymes

Intervention Type: DRUG

Eligibility Criteria

Inclusion Criteria

• clinical signs of sun damage
• post-auricular regions have been visibly sun exposed

Exclusion Criteria

• history of actinic keratoses or skin cancer on tested site
• active tanning
• currently taking hormonal replacement therapy
• using topical or oral treatments for for photo aging in previous 6 months
• are currently pregnant or lactating

• Minimum Eligible Age: 18 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: Yes

Sponsors

Moy-Fincher-Chipps Facial Plastics and Dermatology

OTHER

Sponsor Role: lead

Responsible Party

Responsibility Role: SPONSOR

Central Contacts

Hiren Kolli, BS

Role: CONTACT

hiren@rodeoderm.com

5626594171

References

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Other Identifiers

144156

Identifier Type: -

Identifier Source: org_study_id