Skin cancer is one of the leading causes of cancer mortality among the youth. Acute sun damage due to long-term exposure to the sun’s maximum ultraviolet radiation (UV) makes skin vulnerable to scarring and progressively growth of skin cancers. In fact, skin cancers are considered the most common cancer in Brazil. Unfortunately, current innovative treatments for skin cancer, like phototherapy and oiliness therapy, are often of limited therapeutic efficacy and potentially poor acceptability. In the current limitations of effective therapeutics, such innovative drugs may become promising alternative agents for combating soon to be established yet to-be-identified critical drug targets for malignant skin cancers.
Although it has been known for decades that skin cancers are often resistant to phototherapy and its associated lipid-rich topical treatments, the mechanism responsible for phototherapy-induced resistance in skin cancer remained unclear even up to this time.
Substantial evidence published in the last decade has shown that UV-induced photolytic pathways are activated in a proportion of normal skin tissues. These pathways therefore constitute targets for ultraviolet (UV)-protected tumor-promoting immune cells. However, the mechanism that triggers topical lipid-rich topical chemotherapies, as well as the mechanism of action(. . . ) remained unknown until now.
Using a special antibody model, a team of researchers led by Princess Margaret Cancer Centre (PLC) professor Antonio Nascimento from the Royal Free University of London and the Novo Nordisk Foundation Center for Basic Metabolic Research (CIBER) in Basel, Switzerland, have discovered a novel mechanism used by UV-resistant tumor-promoting T-cells in epidermal structures to trigger a tumorous growth.
Tumours have many times more enzymes which can cleave lipids and activate their cholesterol producing enzymes as well as self-propagate other harmful processes (lipotoxicity). To counteract lipotoxicity specifically, cells coated with lipid-rich liposomes can use their antioxidant defense system to eliminate free radicals directly during the UV-genetic, early damaging process (early damage).
Matrigel-coated microfiber cloths coated with a polymer known as polystyrene were used in a pre-clinical model for the first time. This novel biomaterial is widely used in the commercial production of substances for medical, industrial and military applications but lacked the unique engineered capabilities that can enhance topical lipid absorption and weeding-plant production. It has been speculated that similar to the bottom-tackling method employed in mammals (e. g. dentistry) this also could be applied to manufacture topical lipoproteins.