Certain cutaneous lesions serve as both precursors of skin cancer and markers for increased risk. The solar or actinic keratosis serves such a role for the nonmelanoma (NMSC) forms of skin cancer (basal cell carcinoma and squamous cell carcinoma). Clinically, these keratoses manifest as rough, scaly, erythematous patches on chronically sun-exposed surfaces. Conversion to squamous cell carcinoma in an individual lesion is uncommon and has been estimated at 1 per 1000 per year. Individuals with actinic keratoses have had sufficient chronic photodamage to produce skin cancer, and regular surveillance is recommended. The second precursor for invasive NMSC is Bowen's disease (squamous cell carcinoma in situ). Invasion of the dermis results in frank squamous cell carcinoma. Some types of viral warts may develop into squamous cell carcinoma. The most important precursor/marker for melanoma is the clinically atypical mole (CAM) or dysplastic nevus. CAMs occur in 5-10% of the U.S. population. CAMs, under photographic follow-up, have been observed to evolve into cutaneous melanoma. The frequency of conversion to melanoma of any single CAM is quite low; however, in melanoma-prone families, prospectively diagnosed melanomas arise in association with a histopathologically observed dysplastic nevus in more than 80% of the cases. Giant congenital melanocytic nevi have an approximately 6% lifetime risk of melanoma development. The risk associated with small congenital nevi is uncertain. Lentigo maligna develop into invasive melanoma with a frequency reported in the literature ranging from 5-50%.