The tumors were scrutinized for (dis-)similarities with tumors induced by two-stage chemocarcinogensis (mostly papillomas with H-Ras mutations instead of SCCs) and skin carcinogenesis by chronic UV exposure (i.e. life-long daily sub-sunburn exposure resulting in SCCs and actinic keratosis as benign precursors, both types of lesions with UV-signature mutations in p53). This evidence concerns the gene HRAS and neoplasm.