No association of high-risk human papillomavirus with esophageal squamous cell carcinomas among Koreans, as determined by polymerase chain reaction.

The incidence of esophageal squamous cell carcinoma varies greatly with race and geographic location. It has been suggested that human papillomavirus (HPV) is involved in the pathogenesis of esophageal cancers, and that the incidence of esophageal cancers associated with HPV depends on the geographic location of the patient population. In studies performed on tumor specimens collected from areas with a low incidence of esophageal squamous cell carcinomas, HPV infection was detected in only a small percentage of tumors, whereas studies performed on specimens obtained from areas with a high incidence of esophageal squamous cell carcinomas provided strong evidence that HPV plays a significant role in esophageal carcinogenesis. To elucidate the putative role of HPV infection in the etiology of esophageal cancer in Korea, a total of 129 formalin-fixed, paraffin-embedded tumor specimens, eight fresh tumor tissues and 40 normal esophageal tissues were screened for HPV infection by polymerase chain reaction using consensus primers for HPV types 16, 18, 31, 33, 35, 52b and 58 and type 16-specific primers. SiHa cell line, formalin-fixed, paraffin-embedded cervical squamous cell carcinoma specimens were used as positive controls for HPV infection. Fragments of human beta-globin gene, which served as the internal controls, were successfully amplified from 102 of the 129 cancer specimens and from all the normal and fresh cancer tissues, while consensus and type 16-specific primers failed to detect HPV DNA sequences in any of the esophageal samples. The DNA extracted from the SiHa cell line and uterine cervical cancers were positive when both the consensus and type-specific primers were used. The results of this study suggest that HPV is not associated with esophageal carcinogenesis in Korea.