Kaposi Sarcoma Pathogenesis: A Triad of Viral Infection, Oncogenesis and Chronic Inflammation
Identifieur interne : 005228 ( Ncbi/Merge ); précédent : 005227; suivant : 005229Kaposi Sarcoma Pathogenesis: A Triad of Viral Infection, Oncogenesis and Chronic Inflammation
Auteurs : Janet L. Douglas [États-Unis] ; Jean K. Gustin [États-Unis] ; Ashlee V. Moses [États-Unis] ; Bruce J. Dezube [États-Unis] ; Liron Pantanowitz [États-Unis]Source :
- Translational biomedicine [ 2172-0479 ] ; 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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PubMed: 23082307
PubMed Central: 3472629
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<front><div type="abstract" xml:lang="en"><p id="P1">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.</p>
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Vaccine and Gene Therapy Institute, Oregon Health Sciences University, Beaverton, OR</aff>
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Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA</aff>
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Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, PA</aff>
<author-notes><corresp id="FN1"><label>*</label>
Corresponding author: Ashlee V. Moses, VGTI-Oregon Health & Science University, 505 NW 185<sup>th</sup>
Ave. Beaverton, OR 97006, Phone: 503-418-2712, <email>mosesa@ohsu.edu</email>
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<abstract><p id="P1">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.</p>
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