据估计，遗传性癌症占全球癌症负担的 10%； 5% 的甲状腺癌被认为是遗传性的。遗传有害基因突变与终生患癌症的高风险相关。致癌基因可通过氧化应激机制增强主要信号通路的激活，从而促进甲状腺癌的发生和进展。确定家族性癌症易感性与甲状腺癌患者氧化应激水平之间可能存在的联系。甲状腺癌患者对癌症（有或没有遗传倾向）进行了调查。研究参与者在有限责任公司（LLC）“肿瘤科学研究中心”（格鲁吉亚第比利斯）接受治疗。研究组于2020年至2021年间收集患者血液中甲状腺激素含量（游离三碘甲状腺原氨酸（fFT3）、游离甲状腺素（fFT4）、结合三碘甲状腺原氨酸（FT3）、结合甲状腺素（FT4）、促甲状腺激素（TSH） ）））和氧化应激强度（非酶抗氧化系统（TAA）的总活性和脂质过氧化产物丙二醛（MDA）的含量）。血液中游离和结合形式的T3和T4水平的差异甲状腺癌患者（第2组和第3组）与对照组（第1组）血清之间差异无统计学意义（F1,2=0.5，p1,2=0.8，F1,3=2.31，p1,3=0.16） 。甲状腺癌患者的 TSH 水平与对照组（第 1 组）相比显着升高（TSH（平均值±标准误差）：第 1 组- 1.21±±0.12，第 2 组-2.45±±0.11（F1,2=107，p1， 2<0.001)，组3-2.47±0.17(F1,3=150，p1,3<0.001))并且MDA水平增加了4-5倍。在来自癌症聚集家族的甲状腺癌患者（第2组）中，TAA水平显着降低（F1 - 2=200；p1 - 2<0.001），在无癌症遗传易感性的患者（第3组）中，TAA水平显着降低（F1 - 2=200；p1 - 2<0.001）。 TAA与对照相比没有变化（F1 - 3=2.13；p1 - 3=0.15），结论：氧化应激在肿瘤发生中起关键作用，抗氧化/氧化剂失衡可能导致正常组织的恶变。在具有癌症家族易感性的患者中，参与氧化代谢调节的多个基因突变可能会导致氧化还原平衡的破坏，增加氧化应激水平，并导致甲状腺癌的发展。© 2024 . 作者。

Hereditary cancer is estimated to account for up to 10% of the worldwide cancer burden; 5% of all thyroid cancers are thought to be genetic. Inheritance of a deleterious mutation in genes associated with a high lifetime risk of developing cancer. Cancer-predisposing genes can promote the initiation and progression of thyroid cancer by enhancing the activation of major signaling pathways through oxidative stress mechanisms.Identification of the possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.Patients with thyroid cancer (with and without genetic predisposition) were investigated. Study participants were treated in Limited Liability Company (LLC) "Oncology Scientific Research Center" (Tbilisi, Georgia). The study group was collected between 2020 and 2021. In patients' blood, the thyroid hormones content (free Triiodothyronine (fFT3), free Thyroxine (fFT4), bound Triiodothyronine (FT3), bound Thyroxine (FT4), Thyroid-stimulating hormone (TSH)), and oxidative stress intensity (total activity of non-enzymatic antioxidant system (TAA) and the lipid peroxidation product, malondialdehyde (MDA), content) were investigated.The difference in free and bound forms of T3 and T4 levels in the blood serum between patients with thyroid cancer (Group 2 and Group 3) and the control group (Group 1) was not statistically significant (F1,2=0.5, p1,2=0.8, F1,3=2.31, p1,3=0.16). In patients with thyroid cancer the TSH level significantly increased compared to the control group (Group 1) (TSH (mean ± Std error): Group 1- 1.21 ± 0.12, Group 2-2.45 ± 0.11 (F1,2=107, p1,2<0.001), Group 3-2.47 ± 0.17 (F1,3=150, p1,3<0.001)) and the MDA levels increased by 4-5 fold. In patients with thyroid cancer from families with cancer aggregation(Group 2), the level of TAA statistically significantly decreased (F1 - 2=200; p1 - 2<0.001), in patients without genetic predisposition to cancer(Group 3), the level of TAA did not change compared to the control (F1 - 3= 2.13; p1 - 3=0.15), CONCLUSIONS: Oxidative stress plays a critical role in tumorigenesis, and antioxidant/oxidant imbalance may contribute to the malignant transformation of normal tissue. In patients with familial susceptibility to cancer mutations of several genes, which are involved in the regulation of oxidative metabolism, may contribute to the disruption of the redox balance, increase the level of oxidative stress, and contribute to the development of thyroid cancer.© 2024. The Author(s).