Our laboratory had identified and confirmed a causal relationship between human cytomegalovirus (hCMV) and human salivary gland (SG) mucoepidermoid carcinoma (MEC). Given that hCMV is commonly resident in SG ductal epithelium, that cancer-related inflammation and its related induction of genetic instability is a hallmark of cancer, and that other herpesviruses are documented oncoviruses, we hypothesized that hCMV would be an important component of MEC pathogenesis. Informed by a revision of Koch's Postulates that speaks to the relationship between viruses and cancer, we satisfied the five causal criteria: (1) hCMV is present in most cases of human MEC; (2) only neoplastic tissue harbors hCMV, not surrounding normal human SG tissue; (3) hCMV-specific gene expression is demonstrable at the human SG cellular level and is positively correlated with human MEC severity; (4) hCMV infection of human MEC cells is correlated and colocalized with an upregulation of a known oncogenic signaling pathway; (5) purified CMV induces malignant transformation (MEC) in SG cells in an in vitro mouse model, and utilizes a pathogenetic pathway similar to hCMV-induced human MEC.
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