Epidermal Precancers and Cancers
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 dysplastic 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 fair-skinned individuals is sunlight, ultraviolet radiation (UVR), and human papillomavirus (HPV). Solar 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.
Epithelial Precancerous Lesions and SCCIS
Dysplasia of epidermal keratinocytes in epidermis and squamous mucosa can involve the lower portion of the epidermis or the full thickness. Basal cells mature into dysplastic keratinocytes resulting in a hyperkeratotic papule, or plaque, clinically identified as “keratosis.” A continuum exists from dysplasia to SCCIS to invasive SCC. These lesions have various associated eponyms such as Bowen disease or erythroplasia of Queyrat, which as descriptive morphologic terms are helpful; terms such as UVR- or HPV-associated SCCIS, however, would be more meaningful but can be used only for those lesions with known etiology.
Epithelial precancerous lesions and SCCIS can be classified into UV-induced [solar (actinic) keratoses, lichenoid actinic keratoses, Bowenoid actinic keratoses, and Bowen disease (SCCIS)], HPV-induced [low-grade squamous intraepithelial lesions (HSIL) and Bowenoid papulosis (SCCIS)], arsenical-induced (palmoplantar keratoses, Bowenoid arsenical) keratosis, and hydrocarbon (tar) keratoses and thermal keratoses.
Solar or Actinic Keratosis
These single or multiple, discrete, dry, rough, adherent scaly lesions occur on the habitually sun-exposed skin of adults. They can progress to SCCIS, which can then progress to invasive SCC (Fig. 11-1). For a full discussion of this condition, see Section 10.
Solar keratoses and invasive squamous cell carcinoma Multiple, tightly adherent dirty looking solar keratoses (see also Figs. 10-25 to 10-27). The large nodule shown here is covered by hyperkeratoses and hemorrhagic crusts; it is partially eroded and firm. This nodule is invasive squamous cell carcinoma. The image is shown to demonstrate the transition from precancerous lesions to frank carcinoma.