Melanoma is the deadliest form of skin cancer because of its propensity to spread beyond the primary site of disease and because it resists many forms of treatment. Incidence of melanoma has been increasing for decades. Although ultraviolet radiation (UV) has been identified as the most important environmental causative factor for melanoma development, UV-protective strategies have had limited efficacy in melanoma prevention. UV mutational burden correlates with melanoma development and tumor progression, underscoring the importance of UV in melanomagenesis. However, besides amount of UV exposure, melanocyte UV mutational load is influenced by the robustness of nucleotide excision repair, the genome maintenance pathway charged with removing UV photoproducts before they cause permanent mutations in the genome. In this review, we highlight the importance of the melanocortin hormonal signaling axis on regulating efficiency of nucleotide excision repair in melanocytes. By understanding the molecular mechanisms by which nucleotide excision repair can be increased, it may be possible to prevent many cases of melanoma by reducing UV mutational burden over time.
|Number of pages||14|
|Journal||Photochemistry and Photobiology|
|State||Published - Jan 1 2017|
Bibliographical noteFunding Information:
We are grateful for support from the National Cancer Institute (R01 CA131075), the Melanoma Research Alliance (MRA) and the Regina Drury Endowment for Pediatric Research. We also acknowledge the technical support of the Markey Research Communications Office for their help in preparing figures for this manuscript and NCI Cancer Center Support Grant (P30 CA177558) of the Markey Cancer Center at the University of Kentucky.
© 2016 The American Society of Photobiology
ASJC Scopus subject areas
- Physical and Theoretical Chemistry