Skin cancer—squamous cell carcinoma

Aetiopathogenesis

SCC is derived from moderately well-differentiated keratinocytes. Ultraviolet (UV) radiation is clearly the strongest predisposing risk factor for this condition. The evidence for this is extensive and includes a direct correlation between average annual UV radiation and risk of SCC; increased incidence with proximity to the equator; high incidence in albinos versus non-albinos in tropical climates; and an association with the development of features of photoageing such as wrinkles. The increased incidence of SCC in the last 25 years parallels an increased exposure to UVA due to both UVB protective sunscreens, which prevent sunburn but prolong exposure to UVA, and the increased use of sunbeds.

Predisposing factors include:

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  chronic actinic damage, accumulating over a lifetime of sun exposure (p. 120); psoralen with ultraviolet A (PUVA) treatment can predispose

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  immunosuppression, e.g. in renal transplant patients (p. 70)

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  X-rays or other ionizing radiation; radiant heat (e.g. from a fire; see erythema ab igne, p. 88)

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  chronic ulceration and scarring (e.g. a burn, lupus vulgaris or discoid lupus erythematosus, genetic blistering diseases)

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  smoking pipes and cigars (relevant for lip lesions)

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  industrial carcinogens (e.g. coal tars, oils)

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  human papilloma (wart) virus

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  genetic factors (e.g. albinos, xeroderma pigmentosum, p. 112).

Pathology

The malignant keratinocytes, which retain the ability to produce keratin, destroy the dermoepidermal junction and invade the dermis in an irregular manner (see Fig. 57.1 ).