“…The ability to discriminate SCC variants based on distinct molecular profiles is of great importance when assessing the risk of progression, as well as the clinical management, of patients with cSCC (13). While immunohistochemistry and western blot studies have identified several abundant proteins differentially expressed between cSCC, actinic keratosis (AK) and Bowen's disease lesions, including cyclin-dependent kinase inhibitor 1B (p27), TP53 (14)(15)(16), serpin A1 (SERPINA1) (17); matrix metalloproteinase (MMP)-2, -7, -9 and -13 (16,18,19); c-myc protein (C-MYC) (20); tenascin-C (TNC) (21); and complement factor-I (CFI) and complement factor-H (CFH) (22,23), these markers have not been useful for classifying cSCC subtypes into clinically meaningful categories. The need for comprehensive molecular profiling of cSCC is clear (24).…”