Spinocellular carcinoma

Most spinocellular carcinoma (SCC) cases occur among elderly patients after sun exposure. In younger patients, it can appear on any skin or mucous surface, especially among those with light skin that easily get sunburnt. The most common tumors are in areas exposed to the sun, such as the scalp, face and especially the lower lip, ear, tongue and the back of the hand. Repeated trauma associated with certain occupations can lead to the appearance of spinocellular carcinoma in other areas.
Primary cutaneous spinocellular carcinoma is a malignant neoplasm of keratinous epidermal cells. Unlike basal cell carcinoma, which has a very low metastatic potential, SCC can metastasize and grow rapidly. The clinical symptoms of SCC vary widely. Commonly, SCC appears as an ulcerated nodule or as a superficial erosion on the skin or lower lip but may also present as a papule or warty plaque. Unlike basal cell carcinoma, telangiectasias are rare. The margins of this tumor may be weakly delimited and adhesion to the underlying structures may occur. SCC can appear anywhere on the body, but frequently occurs on the skin damaged by the sun (forehead, face, ear, scalp, neck and back of the hand).
A related neoplasm, keratoacanthoma, typically appears as a dome-shaped papule with a central keratotic crater, rapidly spreading and regressing without therapy, usually. This lesion can be difficult to differentiate from SCC.
SCC has several premalignant forms (actinic keratosis, actinic cheilitis) and in situ forms (eg, Bowen’s disease) that are limited to the epidermis. Keratosis and actinic cheilitis are hyperkeratotic papules and plaques that appear in areas exposed to the sun. While the potential for malignant degeneration is low for any individual lesion, the risk for SCC increases the larger the number of lesions is. Bowen’s disease presents as an erythematous-crustal plaque that can turn into invasive SCC in about 20% of cases. There is controversy regarding the association of Bowen’s disease with internal malignancies; however, recent data suggest that there is no significant relationship when other predisposing factors (eg, arsenic) are absent. Treatment of premalignant and in situ lesions reduces the subsequent risk of invasive disease.