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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.

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Endometrial cancer (EC) is one of the most common gynecological malignancies in Poland, with well-established risk factors. Genetic instability and molecular alterations responsible for endometrial carcinogenesis have been systematically investigated. The aim of the present study was to investigate, by means of cDNA macroarrays, the expression profiles of genes encoding extracellular matrix (ECM) proteins in ECs. Tissue specimens were collected during surgical procedures from 40 patients with EC, and control tissue was collected from 9 patients with uterine leiomyomas. RNA was isolated and RT-PCR with radioisotope-labeled cDNA was performed. The levels of ECM protein gene expression in normal endometrial tissues were compared to the expression of these genes in EC specimens. Statistically significant differences in gene expression, stratified by clinical stage of the ECs, were detected for aggrecan, vitronectin, tenascin R, nidogen and two collagen proteins: type VIII chain α1 and type XI chain α2. All of these proteins were overexpressed in stage III endometrial carcinomas compared to levels in stage I and II uterine neoplasms. In conclusion, increased expression of genes encoding ECM proteins may play an important role in facilitating accelerated disease progression of human ECs.