RESUMO
PURPOSE: The p53 gene is located on chromosome 17p13 and may play important roles in cell cycle regulation, apoptosis and the regulation of the expression of other genes as well as tumor suppression. In addition, the p53 gene is believed to play an important role in the progression of various human malignant tumors through mutation and overexpression. There have been few studies on loss of heterozygosity (LOH) study on 17p13 in invasive ductal carcinoma. This study evaluated a 17p13 LOH and protein expression in invasive ductal carcinomas and correlated these results with the clinicopathological factors. METHODS: LOH analysis was carried out using a polymerase chain reaction with four polymorphic microsatellite markers (D17S796, TP53, D17S5, D17S513) in 50 surgically resected tumors and their non-tumorous counterparts. The p53 protein expression level was examined using immunohistochemistry. RESULTS: A LOH and protein expression was detected in 66% and 54% of the tumors, respectively. The LOH rates ranged from 26.3% (D17S513) to 33.3% (TP53). There was no detected LOH or protein expression in the non-tumor parts. The LOH results correlate well with the tumor size and stage. The protein expression results correlate well with the tumor histological grade. There was no correlation between the LOH and protein loss. CONCLUSION: 17p13 LOH and p53 gene abnormalities may be associated with tumorigenesis and tumor invasion. In addition, the combined use of both methods may help in early detection as well as for determining the prognosis of an invasive ductal carcinoma. 17p13 LOH and p53 protein expression may contribute to tumor progression through reciprocal complementation in some portions of the invasive ductal carcinoma.