INVESTIGATION OF ESOPHAGEAL ADENOCARCINOMA FOR VIRAL GENOMIC SEQUENCES

Overexpression of the tumour suppressor gene product p53 is common in oesophageal adenocarcinoma. This may be due to gene mutation, but over expression can also result from complexing between viral proteins and p53; a number of viruses are causally linked with malignancy. This stu dy therefore investigated the prevalence in oesophageal adenocarcinoma of viruses whose gene products are capable of interacting with p53. S eventeen tumours and 17 normal oesophagi were screened for specific DN A sequences from human papilloma virus (HPV), Adenovirus type 12, Epst ein-Barr Virus (EBV), and cytomegalovirus (CMV). Frozen sections were analysed by polymerase chain reaction, and results were confirmed by S outhern blot hybridization. Overexpression of p53 was studied immunohi stochemically. Overexpression of p53 was identified in 11 of 17 tumour s. No viral sequences were detected for HPV, CMV, or Adenovirus in any tumour. EBV sequences were found in eight of 17 tumours, and eight of 17 negative controls, There is therefore no evidence of HPV 16, 18 an d 33, Adenovirus 12 or CMV infection in oesophageal adenocarcinoma. EB V infection in the oesophagus is of doubtful significance, in view of the high incidence in the control population. Overexpression of p53 ca nnot be explained by complexing with common viral proteins, and must b e related to other intracellular mechanisms.