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

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

Research output: Contribution to journalArticle

17 Citations (Scopus)

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

Fingerprint

Kaposi's Sarcoma
Virus Diseases
Carcinogenesis
Human Herpesvirus 8
Inflammation
Neoplasms
Tumor Microenvironment
Herpesviridae
Therapeutics
Growth
Infection

ASJC Scopus subject areas

  • Medicine (miscellaneous)

Cite this

Kaposi sarcoma pathogenesis : A triad of viral infection, oncogenesis and chronic inflammation. / Douglas, Janet; Gustin, Jean; Moses, Ashlee; Dezube, Bruce J.; Pantanowitz, Liron.

In: Translational Biomedicine, Vol. 1, No. 2, 2, 2010.

Research output: Contribution to journalArticle

@article{3749ce20610d4c5e88c060b2e8a0c9c1,
title = "Kaposi sarcoma pathogenesis: A triad of viral infection, oncogenesis and chronic inflammation",
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.",
author = "Janet Douglas and Jean Gustin and Ashlee Moses and Dezube, {Bruce J.} and Liron Pantanowitz",
year = "2010",
doi = "10:3823/409",
language = "English (US)",
volume = "1",
journal = "Translational Biomedicine",
issn = "2172-0479",
publisher = "iMedPub",
number = "2",

}

TY - JOUR

T1 - Kaposi sarcoma pathogenesis

T2 - A triad of viral infection, oncogenesis and chronic inflammation

AU - Douglas, Janet

AU - Gustin, Jean

AU - Moses, Ashlee

AU - Dezube, Bruce J.

AU - Pantanowitz, Liron

PY - 2010

Y1 - 2010

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84859642925&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84859642925&partnerID=8YFLogxK

U2 - 10:3823/409

DO - 10:3823/409

M3 - Article

AN - SCOPUS:84859642925

VL - 1

JO - Translational Biomedicine

JF - Translational Biomedicine

SN - 2172-0479

IS - 2

M1 - 2

ER -