A few chronic dermatoses can predispose to the development of SCC, including lichen sclerosis et atrophicus, disseminated and superficial actinic porokeratosis, warts, discoid lupus, long-standing ulcers, and scars. Many genetic diseases can predispose to the development of SCC; two of the best recognized ones are epidermodysplasia verruciformis and xeroderma pigmentosum.
Pathogenesis: SCC is related to cumulative ultraviolet exposure. Ultraviolet B (UVB) light appears to be the most important action spectrum in the development of SCC. UVB is much more potent than ultraviolet A light. UVB can damage keratinocyte DNA by causing pyrimidine dimers and other DNA mutations. The damaged DNA leads to errors in translation and transcription and ultimately can lead to cancer. The p53 gene (TP53) is one of the most frequently mutated genes. This gene encodes a protein that is important in cell cycle arrest, which allows for DNA damage repair and apoptosis of those cells that have been damaged. If the p53 gene is dysfunctional, this critical cell cycle arrest period is bypassed, and the cell is allowed to replicate without the normal DNA repair mechanisms acting on the damaged DNA. This ultimately leads to unregulated cell division and cancer.
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