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.