P53 OVEREXPRESSION AND HUMAN PAPILLOMAVIRUS (HPV) INFECTION IN ESOPHAGEAL SQUAMOUS-CELL CARCINOMAS DERIVED FROM A HIGH-INCIDENCE AREA IN CHINA

Oesophageal epithelium is frequently exposed to various carcinogens an d mutagens, many of which may cause p53 gene mutations.. The epitheliu m can also be infected with human papillomavirus (HPV), the E6 protein of which may complex with p53 protein and facilitate its degradation. To identify HPV infection and p53 overexpression in oesophageal cance r, we performed immunohistochemical analysis using CM-1 anti-p53 antib ody and DNA in situ hybridization with biotinylated HPV DNA probes on paraffin-embedded sections in 36 patients with oesophageal squamous ce ll carcinomas derived from a high-incidence area in northern China. Sa mples from cancer tissue, adjacent epithelia, regional lymph nodes as well as resection margins were examined. p53 protein accumulation was detected in 55.6% (20/36) of cancer samples, in 20% (1/5) of hyperplas tic epithelium, in 20% (2/10) of dysplastic lesions as well as in 67% (2/3) of carcinoma in situ lesions adjacent to invasive carcinomas. HP V DNA sequences were demonstrated in 3 patients (8.3% of the total). T wo of these HPV-posiiive carcinomas were immunohistochemically negativ e for p53 and one was weakly positive. Our results suggest that p53 ov erexpression is frequently found in oesophageal carcinomas and that p5 3 alteration may be an early event in esophageal carcinogenesis. HPV a nd elevated p53 are not mutually exclusive events, instead they can co exist in some oesophageal squamous cell carcinomas.