Expression of bcl-2 and Mutantp53 In Normal, Hyperplastic and Malignant Endometrium
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Apoptosis is a natural, physiological mechanism that leads to death of unwanted cells. bc1-2 is a proto-oncogene that inhibits apoptosis. In contrast, p53 tumor suppressor gene is known to induce apoptosis. The present study aimed to determine bc1-2 and mutant p53, apoptosis-related proteins, quantitatively by using enzyme immunoassay (EL4) method in normal, hyperplastic and malignant endometrium to clarify their possible role in endometrial hyperplasia and carcinogenesis. bc1-2 protein in the proliferative endometrium was significantly higher than the secretory endometrium (Pc 0.01) suggesting that bc1-2 expression in the normal endometrium is under hormonal control and its presence may be important for cell survival. The expression of bc1-2 protein in hyperplastic endometrium was significantly higher (P < 0.01) than the normal and malignant endometrium, but there was no significant difference between bc1-2 protein level in normal and malignant endometrium groups. Thus, it is possible that overexpression of bd-2 may have an early role in the evolution of endometrial hyperplasia but have no apparent role in the progression of hyperplasia to carcinoma. The current results showed significant increases (P < 0.01) in bc1-2 protein levels in the simple hyperplastic (SH) and non-atypical complex hyperplastic (NCH) endometrium as compared to the normal proliferative and atypical complex hyperplastic (ACH) endometrium. 7/12 (58%) of NCH cases but only 1/10 (10%) of ACH cases were above the highest bc/-2 level in the normal cases as a cut off value (X2= 7.12, P < 0.01). The present data showed no significant difference in the expression of mutant p53 by EL4. in normal, hyperplastic and malignant endometrium. So, mutation in p53 may have no role in progression of normal endometrium to hyperplasia or endometrial cancer. There was no significant correlation between the expression of bc1-2 and mutant p53 oncoproteins in normal, hyperplastic and malignant endometrium. It is suggested that mechanisms other than p53 may play a role in the regulation of bc/-2 expression in the endometrial tissue.