ABSTRACT
Kaposi’s sarcoma (KS) is by far the most common malignancy that affects patients with human immunodeficiency virus (HIV) infection (1). The risk for Kaposi’s sarcoma in persons with HIV infection is approximately 13,000 times the risk for non-HIV-infected persons and can occur at any stage of HIV infection (1-4). The complex biology of this tumor has challenged many scientists over the years. Yet recent advances in molecular virology and a better understanding of cytokine regulation gives rise to hope that therapeutic breakthroughs are imminent. These studies suggest that Kaposi’s sarcoma is the end result of a complicated interplay of cytokines, viruses, angiogenesis, and human genetics. Understanding these elaborate interactions will be the key to improving therapy for this cancer.
