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Summer is the season of picnics, BBQs, family reunions, and graduation parties. With kids enjoying summer break and daylight getting longer, many people take time off for vacation and spend more time outdoors under the hot sun. However, to safely enjoy those long hours outdoors, now is a good time to remind ourselves of ways to prevent skin cancer.
Skin cancer is one of the most frequently diagnosed cancers in the U.S. The most common types of skin cancer are squamous cell carcinoma, basal cell carcinoma, and melanoma, differing in the cell type of origin in the skin (i.e., squamous cells, basal cells, and melanocytes, respectively). Although skin cancer can occur anywhere on the body, it is typically found in areas most commonly exposed to the sun’s ultraviolet (UV) radiation, such as the face, neck, hands, and arms.
The causal link between skin cancer and UV radiation from the sun was first established by a series of experiments performed by dermatologists, physicists, and other biomedical scientists between the 19th and 20th century. Since this discovery, our understanding of the mechanisms underlying sun-induced skin cancer have progressed dramatically.
Yu-Ying He, PhD, associate professor of medicine in dermatology at the University of Chicago, studies the molecular and cellular events that lead to the development of skin cancer.
“Our research addresses the fundamental question of how cells respond to radiation and chemicals from internal or external sources to cause skin cancer,” He said. Her long-term goal is to identify cellular networks that predict one’s susceptibility to skin cancer, thereby enhancing our ability to prevent, detect, and treat skin cancers at earlier stages.
In a study published in Nucleic Acids Research, He’s lab discovered a new piece to the puzzle. They found that the function of the xeroderma pigementosum group C (XPC) protein ― which plays a key role in recognizing and eliminating damaged, cancer-causing DNA ― was controlled by the addition of a molecular tag called phosphorylation. Since XPC is essential for correcting errors in DNA caused by UV radiation through the nucleotide excision repair (NER) pathway, defects in the XPC protein in humans can lead to an increased risk of skin cancer.
He’s data indicate that XPC phosphorylation may represent a new mechanism for regulating the NER pathway after DNA is damaged by UV radiation, a finding that may improve our ability to prevent skin cancer in the future.
Until our understanding of the molecular events that drive skin cancer is complete, an important way to mitigate its devastating effects is through early detection and prevention. In order to detect skin cancer at an early stage, it is imperative to recognize major characteristics of basal and squamous cell carcinoma, and melanoma.