Human papillomavirus is detectable in Barrett's esophagus and esophageal carcinoma but is unlikely to be of any etiologic significance

Abstract

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.