No abstract

Abstract. Human papillomavirus (HpV) is widely accepted as the main cause of cervical cancer. However, the presence of HpV DnA does not inescapably lead to the development of the cancerous phenotype of the infected cell. therefore, it is considered that the induction of full cancerous expression of HpV requires additional cofactors. the aim of this study was to assess the expression of estrogen receptor α (erα) and progesterone receptor (pr) in archived tissue blocks of squamous cell carcinoma and adenocarcinoma of the uterine cervix and to ascertain whether expression of these receptors is associated with the presence of HpV DnA. the investigation was performed using formalin-fixed, paraffin-embedded cervical cancer specimens obtained from 250 women who underwent surgery for histologically confirmed neoplastic lesions. the control group consisted of normal cervical tissues obtained from 50 patients who underwent myomectomy. the results of this study revealed that the expression of er and pr in planoepithelial cancers and adenocarcinomas of the cervix were decreased to undetectable levels. only in singular cases in the pattern of staining the expression of er and pr was noted.In stromal cells of the tested neoplasms, higher expression of both types of receptors was found. comparison of the expression of er and pr in the staining pattern and stroma of both squamous cell carcinoma and adenocarcioma of the cervix, showed statistically higher expression in the stromal cells. strong expression (+1, +2, +3) of er and pr was noted in the stromal cells irrespective of HpV infection, histopathological type of cancer, and clinical and histopathological grade.

MMP-2 may be implicated in pathogenesis of leiomyoma.

Epidermal growth factor receptor (EGFR) expression and EGFR-tyrosine kinase (EGFR-TK) activity were measured in proliferative (n = 12) and neoplastic (n = 31) human endometrium. Immunoreactivity of EGFR was related to clinicopathological features, estrogen receptor (ER) and progesterone receptor (PR) status, and patient outcome. All proliferative and 27 neoplastic specimens expressed the EGFR. Expression of the EGFR was higher in proliferative endometrium than in endometrial cancer (p < 0.0001). ER immunostaining was observed in 19 of the endometrial carcinomas, while PR expression was demonstrated in only 12 neoplastic specimens. EGFR expression was not related to the ER/PR immunostaining in endometrial carcinomas. Clinicopathological features (age, stage, histological type, grade or depth of invasion) and clinical outcome were unrelated to EGFR immunoreactivity. EGFR-TK activity was detected in 29 of 31 endometrial neoplasms with a 9 times higher mean activity in neoplastic than in proliferative endometrial specimens. There was no relationship between the EGFR-TK activity and EGFR immunostaining in human neoplastic endometrium (p = 0.77). A trend towards a poorer outcome of patients with the EGFR-TK activity above 40 pmol/min/mg was observed, but was not statistically significant. These results support the view that the EGFR expression is downregulated in endometrial carcinomas compared to proliferative endometrial specimens.