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. 2010;1(2):172.

Kaposi Sarcoma Pathogenesis: A Triad of Viral Infection, Oncogenesis and Chronic Inflammation

Affiliations

Kaposi Sarcoma Pathogenesis: A Triad of Viral Infection, Oncogenesis and Chronic Inflammation

Janet L Douglas et al. Transl Biomed. 2010.

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.

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Figures

Figure 1
Figure 1
KS plaques of the lower extremity
Figure 2
Figure 2. KS progression: a histological view
A) Patch stage:
  1. subtle proliferation of irregular vascular channels between normal stromal collagen

  2. the extravasation of erythrocytes and hemosiderin into the stroma

  3. detection of lymphoplasmacytic infiltrate

B) Plaque stage:
  1. proliferating spindled cells that form interlacing bundles closely approximated with blood-filled vascular spaces

  2. intracellular hyaline globules within lesional cells (likely representing phagocytosed erythrocytes within lysozomes)

  3. increased inflammatory infiltrate consisting of lymphocytes, plasma cells, macrophages, and dendritic cells

C) Nodular stage:
  1. formation of intersecting fascicles and sheets of proliferating spindled cells

Figure 3
Figure 3
Model of KS tumorigenesis with sites for therapeutic intervention

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