Sullivan Ryan J, Pantanowitz Liron, Dezube Bruce J
Division of Hematology/Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
BioDrugs. 2009;23(2):69-75. doi: 10.2165/00063030-200923020-00001.
Kaposi sarcoma (KS) occurs as a result of Kaposi sarcoma-associated herpesvirus (KSHV) infection, typically in the context of one of several immunodeficient states. In the US, patients with KS may either be co-infected with HIV or receiving immunosuppressant therapy following solid-organ transplantation. Systemic treatment of KS has traditionally involved one of several chemotherapeutic agents administered either in combination or as single agents, which typically provide reasonable response rates and short-term control. However, recurrence of KS is common, and progression-free intervals are under 1 year. For these reasons, new therapies have been sought and with the elucidation of novel pathogenic mechanisms of KS infection, rational therapeutic targets have been identified. These include KSHV replication, restoration of immune competence, and signal transduction pathways utilized by KSHV in the propagation of KS. This review focuses on these emerging targets in the treatment of patients with KS and also highlights important clinicopathologic characteristics.
卡波西肉瘤(KS)是由卡波西肉瘤相关疱疹病毒(KSHV)感染引起的,通常发生在几种免疫缺陷状态之一的背景下。在美国,KS患者可能同时感染HIV,或者在实体器官移植后接受免疫抑制治疗。KS的全身治疗传统上涉及几种化疗药物之一,这些药物可以联合使用或作为单一药物使用,通常能提供合理的缓解率和短期控制。然而,KS复发很常见,无进展生存期不到1年。由于这些原因,人们一直在寻找新的治疗方法,随着KS感染新致病机制的阐明,已经确定了合理的治疗靶点。这些靶点包括KSHV复制、免疫能力恢复以及KSHV在KS传播中利用的信号转导途径。本综述重点关注KS治疗中这些新兴靶点,并突出重要的临床病理特征。