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Cutaneous epithelial cancers (nonmelanoma skin cancer [NMSC]) originate most commonly in the epidermal germinative keratinocytes or adnexal structures. The two principal NMSCs are basal cell carcinoma (BCC) and squamous cell carcinoma (SCC). SCC often has its origin in an identifiable in situ lesion that can be treated before frank invasion occurs. In contrast, in situ BCC is not known, but minimally invasive “superficial” BCCs are common.

The most common etiology of NMSC in light-skinned individuals is sunlight (ultraviolet radiation [UVR]), and human papillomavirus (HPV). Solar actinic keratoses are the most common precursor lesions of SCC in situ (SCCIS) and invasive SCC occurring at sites of chronic sun exposure in individuals of northern European heritage (see Section 10). UVR and HPV cause the spectrum of changes ranging from epithelial dysplasia to SCCIS to invasive SCC. Much less commonly, NMSC can be caused by ionizing radiation (arising in sites of chronic radiation damage), chronic inflammation, hydrocarbons (tar), and chronic ingestion of inorganic arsenic; these tumors can be much more aggressive than those associated with UVR or HPV. In the increasing population of immunosuppressed individuals (those with HIV/AIDS disease, solid organ transplant recipients, etc.), UVR- and HPV-induced SCCs are much more common and can be more aggressive.


  • Single or multiple, discrete, dry, rough, or adherent scaly lesions on the habitually sun-exposed skin of adults, usually on a background of dermatoheliosis.

  • Actinic keratoses can progress to squamous cell carcinoma.

  • Synonym: Solar keratosis.


AGE OF ONSET Middle age, although in Australia and southwestern United States, solar keratoses may occur in persons <30 years.

SEX More common in males.

RACE More common in light-skinned people.

OCCUPATION Outdoor workers (especially farmers, ranchers, and sailors) and outdoor sportspersons (tennis, golf, mountain climbing, and deep-sea fishing).


Prolonged and repeated solar exposure in susceptible persons leads to cumulative damage to keratinocytes by the action of UVR, principally UVB (290 to 320 nm).


SKIN SYMPTOMS Lesions may be tender. Painful if excoriated with a fingernail.

SKIN LESIONS Takes months to years to develop. Adherent hyperkeratotic scale, which is removed with difficulty and pain (Figs. 11-1 and 11-2). Rough, like coarse sandpaper, “better felt than seen” on palpation. Most commonly <1 cm, oval or round (Fig. 11-2).


Erythematous and brownish macules and papules with coarse adherent scale became confluent on the bald scalp with dermatoheliosis These hyperkeratosis are yellowish to gray. Early lesions can be better felt than seen. Gentle abrasion with the fingernail is painful, a helpful diagnostic finding.


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