Background

Skin cancer remains the most prevalent type of cancer in the United States, and its burden on the health care system remains substantial. Standard treatments such as cryosurgery, electrodessication and curettage, topical and photodynamic therapies, and surgical excision including Mohs micrographic surgery are not without inherent morbidity, including risk of bleeding, infection, and scar.

Objective

Lasers may be an alternative for treatment of nonmelanoma skin cancer, and this paper reviews this therapeutic option.

Methods

A comprehensive search in the Cochrane Library, MEDLINE, and PUBMED databases was performed to identify relevant literature investigating the role of laser therapy in the treatment of nonmelanoma skin cancer.

Results

New literature regarding laser treatment of nonmelanoma skin cancer is emerging, demonstrating promising clinical outcomes. The greatest efficacy has been seen with vascular-selective and ablative lasers in the treatment of basal cell carcinomas. Some success has been reported for laser treatment of squamous cell carcinoma, but data are less convincing. In summary, laser therapy offers an alternative treatment option for nonmelanoma skin cancer; however, its clinical efficacy is variable and, at this time, remains less than currently accepted standards of care.

Conclusion

Further studies are needed to optimize parameters, determine maximum efficacy, and provide long-term follow-up.

Impaired estrogen receptor α (ERα) action promotes obesity and metabolic dysfunction in humans and mice; however, the mechanisms underlying these phenotypes remain unknown. Considering that skeletal muscle is a primary tissue responsible for glucose disposal and oxidative metabolism, we established that reduced ERα expression in muscle is associated with glucose intolerance and adiposity in women and female mice. To test this relationship, we generated muscle-specific ERα knockout (MERKO) mice. Impaired glucose homeostasis and increased adiposity were paralleled by diminished muscle oxidative metabolism and bioactive lipid accumulation in MERKO mice. Aberrant mitochondrial morphology, overproduction of reactive oxygen species, and impairment in basal and stress-induced mitochondrial fission dynamics, driven by imbalanced protein kinase A-regulator of calcineurin 1-calcineurin signaling through dynamin-related protein 1, tracked with reduced oxidative metabolism in MERKO muscle. Although muscle mitochondrial DNA (mtDNA) abundance was similar between the genotypes, ERα deficiency diminished mtDNA turnover by a balanced reduction in mtDNA replication and degradation. Our findings indicate the retention of dysfunctional mitochondria in MERKO muscle and implicate ERα in the preservation of mitochondrial health and insulin sensitivity as a defense against metabolic disease in women.