Settings. Despite the limited diagnostic utility of AgNORs (argyrophilic nucleolar organiser region-associated proteins) for individual breast lesions, AgNOR analysis bears a significant potential for characterizing cell proliferative activity of breast lesions. Methodology. The present study investigated the relationship between mean AgNORs count and immunohistochemical expression of ER, PR, HER2/neu, and p53 in breast carcinoma in serial paraffin sections from 137 breast carcinomas. Twenty control cases of benign breast lesions were included. Results. Mean AgNOR counts correlated significantly inversely with hormone estrogen receptors (ER), Progesterone receptors (PR), and p53 immunohistochemical expression, denoting values of 0.05, 0.01, and 0.001, respectively. No significant correlation was found between mean AgNOR counts and HER2/neu, . Mean AgNOR count was significantly higher in grade II tumor cells. We conclude that mean AgNOR counts correlate with ER, PR, and P53 tumor markers in breast carcinomas. Conclusion. We recommend the use of mean AgNOR count for accurate reporting of breast carcinomas, as well as prediction of ER, PR, and P53 in routine paraffin sections. 1. Introduction Breast cancer is the top cancer in women both in the developed and the developing world [1]. Breast cancer survival rates vary greatly worldwide, ranging from 80% or over in North America, Sweden, and Japan to around 60% in middle-income countries and below 40% in low-income countries [2]. The low survival rates in less developed countries can be explained mainly by the lack of early detection programmes, resulting in a high proportion of women presenting with late-stage disease, as well as by the lack of adequate diagnosis and overall management facilities [1]. Since breast cancer is one of the hormone-dependent tumors much attention has been paid to the relationship between ER and PR and breast cancer. The study by Blanco et al. [3] showed that ER+ PR+ patients had better prognosis than ER? PR? patients. In late 1970s and early 1980s, the measurement of ER as well as PR became standard practice in the prediction of the outcome of breast cancer patients [4]. Early observations after the identification of the p53 protein suggested that p53 functioned as an oncogene. In fact, it does, but only in the mutated form. In the late 1980s, however, several discoveries proved that the normal function of p53 was antioncogenic. One of the several functions of the normal p53 gene is suppression of cell proliferation. When DNA is damaged, p53 inhibits the progression of cell cycle
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