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JNCI Journal of the National Cancer Institute 2000 92(9):677-679; doi:10.1093/jnci/92.9.677
© 2000 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 92, No. 9, 677-679, May 3, 2000
© 2000 Oxford University Press

EDITORIALS

Addressing Controversies Over Kaposi's Sarcoma

Robin Weiss, Chris Boshoff

Affiliation of authors: The Cancer Research Campaign (CRC) Viral Oncology Group, Department of Oncology, University College London, U.K.

Correspondence to: Chris Boshoff, M.R.C.P., Ph.D., The CRC Viral Oncology Group, Department of Oncology, 91 Riding House St., University College London, London, U.K. W1P 6BT (e-mail: c.boshoff@ucl.ac.uk).

Kaposi's sarcoma has emerged from being a rarity to being the most important neoplasm in many sub-Saharan countries. Most investigators involved in Kaposi's sarcoma research now agree that the gammaherpesvirus human herpesvirus 8 (HHV8), also called Kaposi's sarcoma-associated herpesvirus (KSHV), is central in the pathogenesis of this disease (1,2). Molecular and seroepidemiologic studies (3,4) have confirmed the association between HHV8 and Kaposi's sarcoma. However, the role of HHV8 in the initiation and maintenance of proliferation of Kaposi's sarcoma tumor cells (spindle cells) remains unclear. Before the discovery of HHV8 (5), it was thought that cellular cytokines, growth factors, and the human immunodeficiency virus-1 (HIV-1) Tat protein initiate and promote the growth of Kaposi's sarcoma spindle cells (6). The fact that the incidence of . . . [Full Text of this Article]

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