Introduction. Malignant transformation of sex-steroid dependent tissues is
associated with the loss of expression of sex steroid receptors as well as of
the tumor suppression gene p53. The aim of this study is to evaluate the
expression of sex-steroid receptors, p53 and Ki-67 in specimens from
pre-malignant and malignant cervical epithelial lesions throughout the
menstrual cycle. Material and Methods. Immunohistochemical staining was
performed on formalin fixed, paraffin embedded tissue sections of normal
squamous cervical epithelium, cervical intraepithelial neoplasia and invasive
squamous cervical carcinoma, specimens utilizing antibodies against estrogen
receptors, progesterone receptors, p53 protein and Ki-67 antigen. Results. In
the samples taken from the normal cervical tissue, basal cells were usually
estrogen receptor-positive, progesterone receptornegative, p53-negative and
Ki-67-negative throughout the menstrual cycle. In contrast, para-basal cells
were estrogen receptorpositive and progesterone receptor-negative in the
follicular phase, but estrogen receptor-negative and progesterone receptor
-positive and Ki-67 positive in the luteal phase. In cervical precancerous
and cancer tissue samples (cervical intraepithelial neoplasia and squamous
cervical carcinoma), the expression of estrogen receptors decreased. 31.15%
of cervical intraepithelial neoplasia and 11.5% of squamous cervical
carcinoma were positive for estrogen receptors. However, the expression of
progesterone receptors increased. 29.5% of cervical intraepithelial neoplasia
and 49.2% of squamous cervical carcinoma were positive for progesterone
receptors. Positive staining for p53 was observed in 15 (24.59%) cases of
cervical intraepithelial neoplasia and in 39 (64%) of squamous cervical
carcinoma. The expression Ki-67 index in squamous cervical carcinoma cases
(47.60%) was significantly higher than of cervical intraepithelial neoplasia
cases (30.2%) (p=0.041). Conclusion. The findings of this study suggest that
tumor cervical cells evade normal growth control by sex steroid hormones
while synchronously abnormal regulatory mechanisms acquire control of the
cell cycle.