Immunosuppressive cytokines are the main components of the tumor microenvironment and perform a vital function in controlling the immune response to malignant neoplasms.The objective: to study the influence of interleukin-4 (IL-4) and transforming growth factor-β3 (TGF-β3) on the development of breast tumors in women.Materials and methods. The concentration of cytokines IL-4 and TGF-β3 in blood serum was determined in 40 women with benign breast tumors, 40 women with malignant breast tumors, and 40 healthy patients without breast pathology, who were included in the control group.Breast cancer (BC) patients were divided into two groups; the first group included patients with the II stage of BC, who were considered to have a low level of BC, and the second group included patients with III and IV stages of BC, who were considered to have a high level. The method of solid phase immunoenzymatic analysis was used to determine the level of cytokines.Results. The results showed that women with benign breast tumors (86.82±1.67 pg/ml) had no statistically significant difference in IL-4 levels compared to the control group (88.25±1.56 pg/ml). However, a significantly higher level of IL-4 (P=0.0001) was found in women with BC (97.12±1.84 pg/ml) compared to the control group.In addition, the results showed that the concentration of TGF-β3 did not increase significantly in women with benign breast tumors (80.84±2.88 pg/ml) compared with patients with BC and controls (80.84±2.88 and 87.89±2.41 pg/ml, respectively). However, the level of TGF-β3 was significantly higher (P=0.01) in women with BC compared to the control group.Conclusions. The results of the current study indicate that the concentrations of TGF-β3 and IL-4 in the blood serum of women may be useful predictors for the early detection of breast cancer, as well as serve as a prognostic indicator of its development.
Autorías: Hadeer Idan Ghanim, Ishraq Mahmood. Localización: Revista iberoamericana de psicología del ejercicio y el deporte. Nº. 3, 2021. Artículo de Revista en Dialnet.
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