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The relationship between simian virus 40 and mesothelioma

Rivera, Zeyanaa; Strianese, Orianaa,b; Bertino, Pietroa,c; Yang, Haininga; Pass, Harveyd; Carbone, Michelea

Current Opinion in Pulmonary Medicine: July 2008 - Volume 14 - Issue 4 - p 316–321
doi: 10.1097/MCP.0b013e3283018220
Diseases of the pleura: Edited by Richard W. Light

Purpose of review Simian virus 40 is present in some human malignant mesotheliomas. The evidence in favor and against a pathogenic role of simian virus 40 in malignant mesothelioma is discussed in this review.

Recent findings When simian virus 40 is injected intracardially into hamsters, 60% develop and die of malignant mesothelioma. Moreover, some human malignant mesotheliomas contain and express simian virus 40 DNA and proteins. To date, over 50 laboratories have detected simian virus 40 in malignant mesotheliomas and in other tumors; however, the variability of the percentage of positivity led to a controversy about the role and significance of simian virus 40 in malignant mesotheliomas. Compared with other cell types, human mesothelial cells are unusually susceptible to simian virus 40-induced malignant transformation. The presence of simian virus 40 in malignant mesothelioma has been associated with the activation of specific oncogene pathways. Cocarcinogenesis between simian virus 40 and asbestos in causing malignant mesotheliomas has been demonstrated in three separate research laboratories using different experimental approaches. Epidemiological data possibly linking simian virus 40 and malignant mesothelioma is lacking owing to unattainable identification of infected from noninfected cohorts.

Summary Available evidence appears sufficient to link simian virus 40 either alone or in conjunction with asbestos in causing malignant mesotheliomas; however, it is still insufficient to speculate about the contribution of simian virus 40 to the overall incidence of malignant mesotheliomas.

aCancer Research Center of Hawaii and Department of Pathology, University of Hawaii, Honolulu, Hawaii, USA

bDepartment of Health Sciences, University of Genoa, Genoa, Italy

cDISCAFF Department and DFB Center, University of Piemonte Orientale ‘A. Avogadro’, Novara, Italy

dDepartment of Cardiothoracic Surgery, New York University School of Medicine, New York, New York, USA

Correspondence to Michele Carbone, MD, PhD, 651 Ilalo St., BSB Room 231, Honolulu, HI 96813, USA Tel: +1 808 440 4596; e-mail: mcarbone@crch.hawaii.edu

© 2008 Lippincott Williams & Wilkins, Inc.