Receptor Status of Tumor Cells and Mechanisms of Disorders of Tissue Homeostasis in Carcinogenesis of Serous Ovarian Cancer

The aim of the study is to define the value of sex hormone receptors expression level in serous ovarian cancer tumor cells for different variants of genetic instability of the cellular substrate and to evaluate its pathogenetic role in the biological "behavior" of the tumor.

Material and methods. The study of surgical and biopsy material from 89 patients with serous ovarian cancer was performed in histological preparations stained with hematoxylin and eosin and by the Felgen method. Subsequently, the degree of histological differentiation, mitotic regime and ploidy of tumor cells was evaluated, as well as immunohistochemical analysis of the expression in tumor cells of the tumor suppressor mtp53, progesterone and estrogen receptors. Two study groups were distinguished. The first group consisted of 62.9% of patients with negative p53 IGH status. The second group included 37.1% of cases with positive IGH expression of p53 in cells of serous ovarian cancer.

Results. The first group of the studied tumors was characterized by significant morphological heterogeneity. On the contrary, in the group of serous carcinomas where a pronounced expression of oncogen p53 was diagnosed with a pronounced tendency to a low degree of histological differentiation of the parenchymal component of the tumor showed much greater morphological similarity and uniformity. At the same time, tumors in this group were characterized by the maximum indicators of ploidy of tumor cells, which, in our opinion, indicates an increase in cellular atypism and pronounced genetic instability against the background of high proliferative activity. With a significantly different level of genetic instability between the carcinomas of the study groups, the expression of estrogen receptors showed an inverse dependence on the level of cell proliferative activity and the amount of genetic material in the cancer cell. A negative correlation of the level of expression of sex hormone receptors with the degree of tumor differentiation regardless of the level of genetic abnormalities was revealed.

Conclusion. It has been shown that the potential of tumor progression and the clinically more aggressive behavior of a neoplastic tissue substrate largely depends on the level of genetic instability in the epithelium of a cancer tumor, but at the same time, the altered regulatory mechanisms of cellular interactions (dysfunction of paracrine and endocrine regulation) in the tumor type cells leading to a violation of tissue homeostasis.

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