LOSS OF HETEROZYGOSITY AT 17p13 IN GASTRIC CANCER AND COLORECTAL CANCER

Southern hybridization was done on DNA samples of22 gastric tumors and corresponding normal tissues, 14colorectal tumors and corresponding normal tissues by probe phs53B mapping at 17P13.1 and probe PYNZ22mapping at 17pl3.3 which were purchased from the American Type Culture Collection. RFLP heterozygosity was observed in 12 normal tissues of gastric cancers and 10 normal tissues of colorectal cancers. Among these informative tumors, 6(50%) cases of gastric cancers and 6(60%) cases of colorectal cancers showed the loss of beterozygosity at 17p13. Our results demonstrated that the inactivation of wild type p53 might be involved in the carcinogenesis of gastric cancers and colorectal cancers.Furthermore, the mode of inactivation of p53 was in accord with the "two hits" hypothesis by Anudson. The signincance was discussed regarding the presence of LOH detected by probe PYNZ22 mapping at 17pl3.3.