asal cell carcinoma (BCC) is the most common human cancer.' Although rarely metastatic, it is capable of extensive local growth that can result in significant cosmetic and functional impairment.This article reviews what is known of the etiology and pathogenesis of BCC, including those factors that predispose to its development, its apparent sites of origin within the skin, and how its development differs, in some important biologic respects, from the development of cutaneous squamous cell carcinoma (SCC). Predisposing Agents Ul truviolet LightEvidence linking BCC development with sun exposure is strong.Increased BCC incidence is seen in individuals with fair skin,2,3 poor tanniy ability,2,4 blond hair,2,3 blue eyes,2 increased agel male sex,24 and significant lifetime sun exposure.2,3,7In population studies, BCC incidence varies directly with proximity to the equator,4r8 where the ultraviolet B content of sunlight is greatest.The action spectrum of ultraviolet light in BCC production, specifically, has not been studied; ultraviolet B (280-320 nm) has been shown to be a cutaneous carcinogen in many animal studies,'-I' and ultraviolet A (320400 nm) is both a potentiator of ultraviolet B's carcinogenic effects12,13 and a primary cutaneous carcinogen in its own right.14/15These studies in animals, however, have resulted almost exclusively in SCC and not BCC production.Several lines of evidence suggest that BCC development does not correlate as directly with cumulative sun exposure as SCC does.SCC incidence rates have been shown to rise more rapidly than those of BCC with increasing patient age,16 increasing proximity to the e % uator,16,17 and increased ultraviolet B exposure.lZ*8~19 In addition, the development of BCC at different body sites2,3,5,6,20 does not correlate exactly with either the clinically estimated5j6 or actually mea-sured21,22 amount of ultraviolet exposure received by those sites.
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Stanley J. Miller (1995) studied this question.
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