KAPOSI'S SARCOMA (KS) has long been a clinical and therapeutic challenge. In the century since Moritz Kaposi's first description of this disease in elderly eastern European men, a number of clinical variants have been described along with multiple theories to explain its distribution in various unique and seemingly unrelated populations. To this day, there is still debate about the cell of origin of KS, the role of infectious agent(s), and even whether KS is a genuine malignancy or merely a reactive hyperplasia. A variety of antitumor approaches have been used,1,2 but optimal therapy may depend on answers to some of the more basic questions about the cause and pathogenesis of KS.
Epidemiology offers the first clues. The seemingly disparate groups (classic KS; endemic, both in central Africa and, recently, Greece3; human immunodeficiency virus (HIV)-associated KS; and KS in otherwise immunosuppressed individuals) can best be explained by the notion
Myskowski PL. Kaposi's Sarcoma: Where Do We Go From Here? Arch Dermatol. 1993;129(10):1320–1323. doi:10.1001/archderm.1993.01680310090016
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