Kaposi sarcoma pathogenesis: A triad of viral infection, oncogenesis and chronic inflammation

Janet L. Douglas, Jean K. Gustin, Ashlee V. Moses, Bruce J. Dezube, Liron Pantanowitz

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

Kaposi sarcoma (KS) is a complex cancer that arises from the initial infection of an appropriate endothelial or progenitor cell by Kaposi Sarcoma Herpesvirus/Human Herpesvirus-8 (KSHV/HHV8). However, the majority of KS cases occur when infected patients also suffer from some coincident form of immune deregulation, providing a favorable microenvironment for tumor development. Cellular hallmarks of KS progression include both the hyper-proliferation of KSHV-infected cells and the infiltration of immune modulatory cells into KS lesions, which together result in chronic inflammation, the induction of angiogenesis and tumor growth. This review describes the current understanding of the interactions between KSHV and host responses that result in this unusual cancer, along with existing treatments and prospects for future therapeutic approaches.

Original languageEnglish (US)
Article number2
JournalTranslational Biomedicine
Volume1
Issue number2
DOIs
StatePublished - 2010

ASJC Scopus subject areas

  • Medicine (miscellaneous)

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