P53 MUTATIONS IN ESOPHAGEAL TUMORS FROM A HIGH-INCIDENCE AREA OF CHINA IN RELATION TO PATIENT DIET AND SMOKING HISTORY

Esophageal tumors from 29 patients residing in Guangzhou, China were e xamined for mutations in exons 5-8 of the p53 tumor suppressor gene an d for p53 protein accumulation in tumor cell nuclei, Anamnestic data f or each patient, which included information on family history of cance r, tobacco smoking, drinking of alcoholic beverages, and dietary habit s such as consumption of pickled vegetables, were recorded, Screening of DNA from tumor cells microdissected from biopsies was performed by PCR amplification of p53 gene exons 5-8, denaturing gradient gel elect rophoresis analysis, and DNA sequencing, Mutations were identified in 20 of 29 tumors (69%), All tumors harboring a missense mutation in the p53 gene also showed nuclear accumulation of the tumor suppressor pro tein by immunohistochemistry. The most common p53 mutations in these t umors were guanine to adenine (G --> A) transitions (10 of 20 tumors; 50%). We did not find multiple mutations at codon 176, in contrast to Lung et al, in their recent study of esophageal cancer patients from G uangzhou (M. L. Lung et at, Cancer Epidemiol. Biomark. Prev., 5: 277-2 84, 1996). The mutation prevalence was high both in smokers (13 mutati ons in 20 smokers; 65%) and in nonsmokers (7 of 9 tumors with mutation s; 78%), an observation that differs from that of studies in European and North American patients, which demonstrate a much higher prevalenc e of p53 mutations in smokers than in nonsmokers (reviewed in R. Monte sano et at., Int. J. Cancer Predict. Oncol., 69: 225-235, 1996.). Our findings in this pilot study of tumor suppressor gene mutations in pat ients from Guangzhou support a large body of epidemiological observati ons pointing to dietary mutagenic carcinogens peculiar to populations in China at high risk of esophageal cancer.