BACKGROUND: DNA tumor viruses potentially play a role in the development of squamous cell carcinoma of the head and neck (SCCHN). Human papillomavirus is found in up to 50% of SCCHN specimens, and Epstein-Barr virus (EBV) has been detected in nasopharyngeal carcinoma, Burkitt lymphoma, and other lymphomas. However, the role of EBV in nonnasopharyngeal SCCHN has not been thoroughly investigated. METHODS: Twenty-one SCCHN cell lines derived from tumors of various subsites were used to screen for EBV DNA as well as latent viral protein expression. The method of EBV DNA detection was polymerase chain reaction with 3 independent primer sets from distinct regions of the genome. Expression of the viral protein EBNA-1, critical for the maintenance of the viral episome, was monitored by immunofluorescence using an antibody specific for EBNA-1. In addition, 12 paraffin-embedded tumor specimens and adjacent normal tissues were analyzed by polymerase chain reaction. These tumor specimens were further characterized by immunohistochemistry with the use of a mouse monoclonal antibody that recognizes EBNA-1. RESULTS: Little or no EBV DNA was detected in 20 of 21 cell lines or in any of the tumor specimens, while detecting approximately 40 genome copies in a control reaction. Accordingly, these cell lines and specimens were negative for EBNA-1 expression. In 1 cell line derived from an immunosuppressed patient, EBV DNA was detected, and on further examination a small percentage of cells expressed EBNA-1 as shown by immunofluorescence. CONCLUSIONS: Although EBV may not be a major cofactor contributing to the proliferation of SCCHN, the limited initial evidence suggests that EBV may be involved in development of SCCHN in immunosuppressed patients.
BACKGROUND: DNA tumor viruses potentially play a role in the development of squamous cell carcinoma of the head and neck (SCCHN). Human papillomavirus is found in up to 50% of SCCHN specimens, and Epstein-Barr virus (EBV) has been detected in nasopharyngeal carcinoma, Burkitt lymphoma, and other lymphomas. However, the role of EBV in nonnasopharyngeal SCCHN has not been thoroughly investigated. METHODS: Twenty-one SCCHN cell lines derived from tumors of various subsites were used to screen for EBV DNA as well as latent viral protein expression. The method of EBV DNA detection was polymerase chain reaction with 3 independent primer sets from distinct regions of the genome. Expression of the viral protein EBNA-1, critical for the maintenance of the viral episome, was monitored by immunofluorescence using an antibody specific for EBNA-1. In addition, 12 paraffin-embedded tumor specimens and adjacent normal tissues were analyzed by polymerase chain reaction. These tumor specimens were further characterized by immunohistochemistry with the use of a mouse monoclonal antibody that recognizes EBNA-1. RESULTS: Little or no EBV DNA was detected in 20 of 21 cell lines or in any of the tumor specimens, while detecting approximately 40 genome copies in a control reaction. Accordingly, these cell lines and specimens were negative for EBNA-1 expression. In 1 cell line derived from an immunosuppressed patient, EBV DNA was detected, and on further examination a small percentage of cells expressed EBNA-1 as shown by immunofluorescence. CONCLUSIONS: Although EBV may not be a major cofactor contributing to the proliferation of SCCHN, the limited initial evidence suggests that EBV may be involved in development of SCCHN in immunosuppressed patients.