Association of BCL-2 (rs17759659), CTLA- 4 (rs231775), APO-1/Fas (rs2234767) gene polymorphisms with activity of proliferati on and apoptosis in thyroid ti ssue of patients with nodular forms of goiter

Abstract

The purpose was a comparative analysis of apoptosis processes and proliferative activity in the thyroid nodular and pseudonodular tissues of patients with nodular goiter against a background of autoimmune thyroiditis (NGAIT) and thyroid adenoma (TA) and in the morphologically unaltered tissue by studing the expression / density of markers Fas/ FasL, Bcl‑2, p53 and Ki‑67 on the thyrocytes and with counting the number of immunoreactive cells expressing said markers that regulate apoptosis and proliferation for NGAIT and TA, using the immunohistochemical method, taking into account the polymorphism of the genes BCL‑2 (rs17759659), CTLA‑4 (rs231775) and APO‑1/Fas (rs2234767). It has been established that in patients with NGAIT and TA, several links of thyrocytes apoptosis mechanism with the advantage of Fas-induced, associated with the genome of BCL‑2  rs17759659) and almost 6 times weaker with the promoter of the CTLA‑4 gene (rs231775), are activated due to the expression of Fas and FasL on the surface of the cells of the nodular and pseudonodular tissues of the thyroid gland (more often in the carriers of the GG genotype of the BCL‑2 gene — 18.54% and 36.18% respectively), which indicates the
initiation of the external pathway of apoptosis through the caspase mechanism (effector caspase 8).