The effects of sun exposure on the skin and specifically those related to pigmentation disorders are well known. It has recently been shown that blue light leads to the induction of oxidative stress and long-lasting pigmentation. The protective effect of an aqueous extract of Polypodium leucotomos (Fernblock®) is known. Our aim was to investigate the action mechanism of Fernblock® against pigmentation induced by blue light from digital devices. Human fibroblasts (HDF) and murine melanocytes (B16-F10) were exposed to artificial blue light (a 400–500 nm LED lamp). Cell viability, mitochondrial morphology, and the expression of the mitogen-activated protein kinase (MAPK) p38, known markers involved in the melanogenesis pathway, were evaluated. The activation of Opsin-3, a membrane protein sensitive to blue light that triggers the activation of the enzyme tyrosinase responsible for melanogenesis in melanocytes, was also analyzed. Our results demonstrated that pretreatment with Fernblock® prevents cell death, alteration of mitochondrial morphology, and phosphorylation of p38 in HDF exposed to blue light. In addition, Fernblock® significantly reduced the activation of Opsin-3 in melanocytes and the photo-oxidation of melanin, preventing its photodegradation. In sum, Fernblock® exerts beneficial effects against the detrimental impact of blue light from digital devices and could prevent early photoaging, while maintaining skin homeostasis.

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Summary Melanoma is the most aggressive skin tumour, being the leading cause of death from skin cancer. Its incidence has increased more rapidly than for any of the top 10 cancers. A low percentage of patients with metastasis (meaning it has spread to other parts of the body) survive over one year after diagnosis, due to the lack of efficient therapy. Not all melanomas are the same, they can vary in how aggressive they are (how quickly they develop and potentially spread) and in their appearance. The authors of this study, from Spain, studied cultured (grown in the lab from a sample) melanoma cells with different aggressiveness features and patients with different types of melanoma lesions. They aimed to find metabolic markers in melanoma that could predict the evolution of the disease. Cellular metabolism is the set of chemical reactions that occur in living organisms in order to maintain life. It is known that the metabolism of cancer cells is different from that of normal cells since they grow and divide rapidly, needing high‐energy supply. In this context, the authors found that proteins (enzymes) related with energy production are altered. These proteins are: the ATP synthase (β‐F1‐ATPase), the heat‐shock protein 60 (HSP60), the glycolytic glyceraldehyde‐3‐phosphate dehydrogenase (GAPDH) and the pyruvate kinase M2 (PKM2). These proteins provide the bioenergetic signature (BEC index=β‐F1‐ATPase/HSP60/GAPDH ratio) of cancer. A reduction in BEC index correlates with the aggressiveness of cultured melanoma cells and tumours and worse overall survival in melanoma patients. The authors conclude that the level of metabolic enzymes and BEC status are markers of (indicators of) melanoma stage (how adavanced it is, e.g. if it has spread and by how much) and overall survival in melanoma patients.

Squamous cell carcinomas arise from stratified squamous epithelia. Here, a comparative analysis based on recent studies defining the genetic alterations and composition of the stroma of oral and cutaneous squamous cell carcinomas (OSCC and CSCC, respectively) was performed. Both carcinomas share some but not all histological and genetic features. This review was focused on how mutations in tumor suppressor genes and protooncogenes cooperate to determine the differentiation, aggressiveness, and metastatic potential of OSCC and CSCC. In fact, driver mutations in tumor suppressor genes are more frequently observed in OSCC than CSCC. These include mutations in TP53 (encoding pP53 protein), CDKN2A (encoding cyclin dependent kinase inhibitor 2A), FAT1 (encoding FAT atypical cadherin 1), and KMT2D (encoding lysine methyltransferase 2D), with the exception of NOTCH (encoding Notch receptor 1), whose mutation frequency is lower in OSCC compared to CSCC. Finally, we describe the differential composition of the tumor microenvironment and how this influences the aggressiveness of each tumor type. Although both OSCC and CSCC tumors are highly infiltrated by immune cells, high levels of tumor-infiltrating lymphocytes (TILs) have been more frequently reported as predictors of better outcomes in OSCC than CSCC. In conclusion, OSCC and CSCC partially share genetic alterations and possess different causal factors triggering their development. The tumor microenvironment plays a key role determining the outcome of the disease.