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. |
