title: An immunohistochemical analysis of sex-steroid receptors, tumor suppressor gene p53 and Ki-67 in the normal and neoplastic uterine cervix squamous epithelium.
abstract: BACKGROUND
  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.
  
  
  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 receptor-negative, p53-negative and Ki-67-negative throughout the menstrual cycle. In contrast, para-basal cells were estrogen receptor-positive 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).
  
  
  CONCLUSIONS
  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.
authors.forename: Marinos
authors.initials: M
authors.lastname: Nikolaou
authors.forename: Dimitra
authors.initials: D
authors.lastname: Koumoundourou
authors.forename: Panagiota
authors.initials: P
authors.lastname: Ravazoula
authors.forename: Margarita
authors.initials: M
authors.lastname: Papadopoulou
authors.forename: Georgios
authors.initials: G
authors.lastname: Michail
authors.forename: Georgios
authors.initials: G
authors.lastname: Decavalas
mesh_terms: D002294:Carcinoma, Squamous Cell / Q000737:chemistry; D002471:Cell Transformation, Neoplastic; D002584:Cervix Uteri / Q000737:chemistry*; D004848:Epithelium / Q000737:chemistry; D005260:Female; D016158:Genes, p53; D006801:Humans; D007150:Immunohistochemistry; D019394:Ki-67 Antigen / Q000032:analysis*; D011960:Receptors, Estrogen / Q000032:analysis*; D011980:Receptors, Progesterone / Q000032:analysis*; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000235:genetics; D002583:Uterine Cervical Neoplasms / Q000737:chemistry*; D002578:Uterine Cervical Dysplasia / Q000737:chemistry
chemical_list: D019394:Ki-67 Antigen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D016159:Tumor Suppressor Protein p53