Article
Lab Invest 2000, 80:1121–1126
Presence of Human Herpesvirus-8 DNA Sequences and Overexpression of Human IL-6 and Cyclin D1 in Inflammatory Myofibroblastic Tumor (Inflammatory Pseudotumor)
This work was partially supported by grants from the Spanish Ministry of Health (FIS 97/1119) and the Fundación "Marqués de Valdecilla." The Fundación "Marcelino Botín" supported equipment costs (genetic analyzer and PCR systems) at the Department of Immunology.
The contents of this work have been partially presented in EUROCELLPATH'99 in Paris, France, June 24–28, 1999.
José Javier Gómez-Román1, Gonzalo Ocejo-Vinyals2, Pablo Sánchez-Velasco2, Emilia Hernández Nieto1, Francisco Leyva-Cobián2 and José Fernando Val-Bernal1
- 1Departamento de Anatomía Patológica, Hospital Universitario Marqués de Valdecilla, Instituto Nacional de la Salud, Facultad de Medicina, Universidad de Cantabria, Santander, Spain
- 2Servicio de Inmunología, Hospital Universitario Marqués de Valdecilla, Instituto Nacional de la Salud, Facultad de Medicina, Universidad de Cantabria, Santander, Spain
Correspondence: Dr. J. Fernando Val-Bernal, Departamento de Anatomía Patológica, Hospital Universitario Marqués de Valdecilla Avda Valdecilla s/n 39008 Santander, Spain. Fax: 34 942 201903; E-mail: apagrj@humv.es
Received 17 April 2000.
Abstract
Inflammatory myofibroblastic tumor (IMT) is composed of myofibroblasts, plasma cells, and lymphocytes. Cytokines are possibly involved in its pathogenesis. Human herpesvirus-8 (HHV-8) encodes cell cycle regulatory and signaling proteins. A combination of nested PCR with several negative controls and Southern blot methods showed the presence of HHV-8 DNA in seven cases of IMT. Additionally, strong expression was demonstrated by in situ hybridization in many tumoral nuclei. Most of the myofibroblasts in all of the cases were immunoreactive for human IL-6 and cyclin D1. These cytokines probably have a paracrine action and may sustain myofibroblastic growth. HHV-8 could play an essential role in triggering IMT development by a local reactivation of viral lytic replication. The relationship between HHV-8 and immunosuppression status as the only associated cause for tumorigenesis should be revised.
