Kaposi sarcoma.

Radu O, Pantanowitz L.

Source

From the Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.

Abstract

Kaposi sarcoma (KS) is a low-grade vascular tumor associated with Kaposi sarcoma herpesvirus/human herpesvirus 8 (KSHV/HHV8) infection. Kaposi sarcoma lesions predominantly present at mucocutaneous sites, but may involve all organs and anatomic locations. Recognized epidemiologic-clinical forms of KS include classic, African (endemic), AIDS-associated (epidemic), and iatrogenic KS. New clinical manifestations have been described, such as antiretroviral therapy-related KS regression or flares. Kaposi sarcoma lesions evolve from early (patch stage) macules into plaques (plaque stage) that grow into larger nodules (tumor stage). Newer histologic variants include anaplastic, hyperkeratotic, lymphangioma-like, bullous, telangiectatic, ecchymotic, keloidal, pyogenic granuloma-like, micronodular, intravascular, glomeruloid and pigmented KS, as well as KS with sarcoidlike granulomas and KS with myoid nodules. Latency-associated nuclear antigen (HHV8) is the most specific immunohistochemical marker available to help distinguish KS from its mimics. Since KS remains one of the most common AIDS-defining malignancies, it is important that pathologists be able to recognize KS and its contemporary manifestations.

Archives of Pathology and Laboratory Medicine

For the Future Studies of Kaposi’s Sarcoma-Associated Herpesvirus

2012

Keiji Ueda

It is 18 years since Kaposi’s sarcoma-associated virus (KSHV), also called human herpesvirus 8 (HHV-8), was found from Kaposis’ sarcoma (KS) by Chang et al. (1994). More than 8, 000 reports have been published so far and we have learned many things from this virus. I would like to say it is about time to look back previous studies and to think what to study next on the virus, and planed a topic to think what to study next on the virus for future.

Herpesviruses have relatively big genomes and encode a 100 genes or so. Thus, the virion assembly/structure, gene expression regulation and attachment/entry are complicated and have known only an iceberg of them. Studying the details how the viruses run their life cycles and cause diseases in their processes will lead to exploring new therapeutic drugs/methods.

A viral life cycle starts from attachment on the susceptible cells and then, entry into the cells, followed by the viral gene expression, the genome replication, the particle assembly and finally the daughter viruses egress out of the cells. This process is skillfully built and all the viral genes are required for the process, though there are essential genes and non-essential ones. Viral pathogenesis could be established during this process by the interaction between viruses and host cells, and individual host systems such as immune system. In this topic, although I would like to cover all the processes, thankfully, 15 specialists in each field have contributed for this topic.

see full text article:  NIH

Instigation of Notch signaling in the pathogenesis of Kaposi's sarcoma-associated herpesvirus and other human tumor viruses.

Oct 2012

Cheng F, Pekkonen P, Ojala PM.

Source

Institute of Biotechnology & Research Programs Unit, Genome-Scale Biology, University of Helsinki, PO Box 56 (Viikinkaari 9), 00014 University of Helsinki, Helsinki, Finland.

Abstract

The Notch pathway is a highly conserved signaling circuit with a critical role in cell-fate determination and tumor initiation. Notch is reported to regulate various key events in tumor progression, such as angiogenesis, maintenance of cancer stem cells, resistance to therapeutic agents and metastasis. This review describes the intimate interplay of human tumor viruses with the Notch signaling pathway. Special attention is paid to Kaposi's sarcoma-associated herpesvirus, the etiological agent of Kaposi's sarcoma and rare lymphoproliferative disorders. The past decade of active research has led to significant advances in understanding how Kaposi's sarcoma-associated herpesvirus exploits the Notch pathway to regulate its replication phase and to modulate the host cellular microenvironment to make it more favorable for viral persistence and spreading.

Future Medicine