BSBeata Smolarz
Papers(3)
Ovarian Cancer—Epidem…The Immunohistochemic…Study of Estrogen Rec…
Collaborators(4)
Christopher Kobierzyc…Honorata ŁukasiewiczAleksandra PiotrowskaAneta Popiel-Kopaczyk
Institutions(3)
Polish Mothers Memori…Wroclaw Medical Unive…Calisia University - …

Papers

Ovarian Cancer—Epidemiology, Classification, Pathogenesis, Treatment, and Estrogen Receptors’ Molecular Backgrounds

Global epidemiological reports indicate a steady increase in the tendency to develop ovarian cancer. The symptoms of ovarian cancer are non-specific, and there is no effective screening tool. Most often, surgery, chemotherapy, and radiotherapy, alone or in combination, are used to treat ovarian cancer. We have a better understanding of the biology of ovarian cancer, the genetic basis of hereditary ovarian cancer, the stage of the disease, and the role of cytoreductive surgery and more effective chemotherapy, which translates into an increase in the percentage of patients who survive 5 years after diagnosis. A growing body of evidence points to the role of genetic factors in the development of cancer. It is known that mutations in the BRCA1 gene are responsible for an increased risk of developing ovarian cancer. The role of other genetic disorders, such as polymorphic variants, in increasing the risk of developing cancer is still being investigated. Ovarian cancer is a hormone-dependent cancer and its steroid hormones are estrogens. Estrogens affect cells through the estrogen receptors ERα and ERβ. An imbalance between ERα and ERβ receptor expression may, therefore, be a key step in estrogen-dependent carcinogenesis. In 60% of cancer cases, significantly elevated levels of ERα receptors are detected. The ERα receptor is encoded by the ESR1 gene, so its polymorphisms can be considered molecular markers of ovarian cancer. This article discusses the epidemiology, pathogenesis, risk factors, genetic testing, treatment, and diagnosis of ovarian cancer, as well as providing an overview of standard treatment approaches and new, targeted biologic therapies.

The Immunohistochemical Expression of Epithelial–Mesenchymal Transition Markers in Precancerous Lesions and Cervical Cancer

In the epithelial–mesenchymal transition (EMT) process, cells lose their epithelial phenotype and gain mesenchymal features. This phenomenon was observed in the metastatic phase of neoplastic diseases, e.g., cervical cancer. There are specific markers that are expressed in the EMT. The aim of this study was to determine the localization of and associations between the immunohistochemical (IHC) expression of TWIST, SNAIL, and SLUG proteins in precancerous lesions and cervical cancer. The IHC analysis disclosed higher expressions of EMT markers in precancerous lesions and cervical cancer than in the control group. Moreover, stronger expression of TWIST, SNAIL, and SLUG was observed in cervical intraepithelial neoplasia grade 3 (CIN3) vs. CIN1, CIN3 vs. CIN2, and CIN2 vs. CIN1 cases (p < 0.05). In cervical cancer, IHC reactions demonstrated differences in TWIST, SNAIL, and SLUG expression in grade 1 (G1) vs. grade 2 (G2) (p < 0.0011; p < 0.0017; p < 0.0001, respectively) and in G1 vs. grade 3 (G3) (p < 0.0029; p < 0.0005; p < 0.0001, respectively). The results of our study clearly showed that existing differences in the expression of the tested markers in precancerous vs. cancerous lesions may be utilized in the diagnosis of cervical cancer. Further studies on bigger populations, as well as in comparison with well-known markers, may improve our outcomes.

Study of Estrogen Receptor Alpha Gene Polymorphisms (ERα, ESR1) in Women with Ovarian Cancer

Despite the growing knowledge about ovarian cancer, it has not yet been possible to develop an effective screening test for this cancer. Therefore, it seems necessary to identify new risk factors, such as genetic polymorphisms. The aim of this study was to demonstrate whether polymorphisms of the ESR1 gene rs2234693 and rs9340799 may be involved in the development of ovarian cancer. The material for the study was DNA obtained from 100 ovarian cancer patients and 100 control groups. Polymorphisms were determined using the PCR-RFLP technique. The presence of the CC genotype (rs2234693) has been shown to more than double the risk of ovarian cancer (OR 2.21; p = 0.041). In the case of the second polymorphism, rs9340799, the carrier of the GG genotype more than doubles the risk of ovarian cancer (OR 2.62 p = 0.031). Analysis of ESR1 gene haplotypes in relation to the rs2234693 and rs9340799 polymorphisms showed that the occurrence of TCAG and CCGG systems may be associated with a significant increase in the risk of ovarian cancer (OR 1.98, p = 0.043 and OR 2.45, p = 0.041, respectively). In the group of patients with ovarian cancer, a correlation was shown between the polymorphisms rs2234693 and rs9340799 in the tissues of ovarian cancers with the lowest stage compared to more advanced ovarian cancers, which may indicate a relationship between these factors and the stage of the tumor. Women’s age had no effect on the prevalence of individual genotypes or the associated risk of disease. Polymorphisms rs2234693 and rs9340799 of the ESR1 gene may be associated with the occurrence of ovarian cancer.

35Works
3Papers
4Collaborators
Breast NeoplasmsEndometriosisCell Line, TumorBiomarkers, TumorLung NeoplasmsOvarian NeoplasmsApoptosis