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γ‐Herpesvirus neoplasia: A growing role for COX‐2
Author(s) -
Shelby Bryan D.,
Nelson Anne,
Morris Cindy
Publication year - 2005
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/jemt.20226
Subject(s) - primary effusion lymphoma , lymphoma , virus , angiogenesis , sarcoma , epstein–barr virus , cancer research , kaposi's sarcoma associated herpesvirus , biology , medicine , pathology , immunology , herpesviridae , virology , viral disease
Both human γ‐herpesviruses, Epstein‐Barr virus (EBV) and Kaposi's sarcoma‐associated herpesvirus (KSHV) induce neoplasia. Burkitt's and Hodgkin's lymphomas harbor EBV sequences, while KSHV has been associated with Kaposi's sarcoma (KS), primary effusion lymphoma (PEL), and multicentric castleman's disease (MCD). Each of these γ‐herpesvirus‐associated malignancies displays typical characteristics of neoplasia, such as angiogenesis and cell survival. One enzyme commonly overexpressed in breast, prostate, and colon cancers is cyclooxygenase‐2 (COX‐2). Recently, COX‐2 overexpression has been reported in herpesvirus infections in vitro. This review will outline potential mechanisms by which COX‐2 may participate in herpesvirus‐induced neoplasia. Microsc. Res. Tech. 68:120–129, 2005. © 2005 Wiley‐Liss, Inc.