Skin cancers, like all solid malignant tumors, require a blood supply in order to grow larger than a few millimeters in diameter. Tumors induce the growth of new capillary blood vessels, a process called angiogenesis, by producing specific angiogenesis-promoting growth factors. So-called ‘precancerous’ lesions of the skin, including as actinic keratoses (AK) and atypical moles, are already angiogenic, as indicated by their higher density of capillaries than surrounding normal skin.

Acute ultraviolet (UV) exposure, such as occurs with sunburn, causes a burst of angiogenesis in the skin. Within hours of sun exposure, levels of angiogenesis stimulators in the skin increase dramatically. The most potent of these are vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF). At the same time, naturally occurring inhibitors of angiogenesis are suppressed.

Acute UV exposure therefore switches the balance of angiogenesis regulators in favor of uncontrolled angiogenesis. New blood vessel growth continues through the progression from pre-cancerous skin lesions to full-blown skin cancer.