Barrett's esophagus (BE), a known precursor of esophageal adenocarcinoma has recently been associated with human papillomavirus (HPV). p16(INK4a) expression is a recognized surrogate marker of HPV infection in the cervix.
Objectives: This study has assessed the possible role of human papillomavirus (HPV) infection in BE and esophageal adenocarcinoma, in the North American population by screening esophageal tissues for HPV by a combination of assays.
Study design: Formalin-fixed, paraffin-embedded blocks from cases of Barrett's esophagus (n=84), esophageal adenocarcinoma (n=36) and normal gastro-esophageal junction (n=29) were examined for HPV by PCR, chromogenic in situ hybridization, and p16(INK4a) immunohistochemistry.
Results: HPV DNA was detected by PCR in 23 of 84 (27.4%) BE cases, 11 of 36 (31%) cases of adenocarcinoma and in 7 of 29 (24%) normal control cases (p=0.82). p16(INK4a) staining was positive in 10 (12%) cases of BE, 15 (42%) cases of adenocarcinoma and 6 (21%) cases of the control group. Positive p16(INK4a) staining was not statistically different between the three groups whether positive or negative for HPV DNA (p=0.91 and p=0.91 respectively). Similarly, negative p16(INK4a) staining did not show a difference between the three groups for whether positive or negative for HPV DNA (p=0.50 and p=0.28, respectively). HPV was not detected by CISH in the adenocarcinomas while in BE and control groups, CISH was non-contributory.
Conclusions: These data suggest that while HPV is detectable in a subset of esophageal lesions and tumors, the HPV detected is unlikely to be of etiologic significance or a factor accounting for the increase in BE and esophageal adenocarcinoma cases in the United States.
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