Possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.

IF 2 4区医学 Q3 ONCOLOGY Hereditary Cancer in Clinical Practice Pub Date : 2024-08-23 DOI:10.1186/s13053-024-00287-3

Ivane Javakhishvili, Kote Mardaleishvili, Maka Buleishvili, Maia Mantskava, Irakli Chkhikvishvili, Sophio Kalmakhelidze, Nina Kipiani, Tamar Sanikidze

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Abstract

Background: 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.

Aim: Identification of the possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.

Methods: 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.

Results: 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 (F_1,2=0.5, p_1,2=0.8, F_1,3=2.31, p_1,3=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 (F_1,2=107, p_1,2<0.001), Group 3-2.47 ± 0.17 (F_1,3=150, p_1,3<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 (F_1 - 2=200; p_1 - 2<0.001), in patients without genetic predisposition to cancer(Group 3), the level of TAA did not change compared to the control (F_1 - 3= 2.13; p_1 - 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.

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甲状腺癌患者的癌症家族易感性与氧化应激水平之间可能存在联系。

背景：据估计，遗传性癌症占全球癌症发病率的 10%；据认为，5% 的甲状腺癌是遗传性的。基因中有害突变的遗传与终生罹患癌症的高风险有关。癌症易感基因可通过氧化应激机制加强主要信号通路的激活，从而促进甲状腺癌的发生和发展。目的：确定甲状腺癌患者的癌症家族易感性与氧化应激水平之间可能存在的联系：方法：对甲状腺癌患者（有遗传倾向和无遗传倾向）进行调查。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。研究小组在 2020 年至 2021 年期间收集数据。研究人员对患者血液中的甲状腺激素含量（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）总活性和脂质过氧化产物丙二醛（MDA）含量）进行了调查：甲状腺癌患者（第 2 组和第 3 组）与对照组（第 1 组）血清中游离型和结合型 T3 和 T4 水平的差异无统计学意义（F1,2=0.5，P1,2=0.8；F1,3=2.31，P1,3=0.16）。与对照组（第 1 组）相比，甲状腺癌患者的促甲状腺激素水平明显升高（促甲状腺激素（平均值 ± 标准误差）：组 1- 1.21 ± 0.12，组 2-2.45 ± 0.11（F1,2=107，P1,21,3=150，P1,31 - 2=200；P1 - 21 - 3= 2.13；P1 - 3=0.15），结论：氧化应激在甲状腺癌患者中起着至关重要的作用：氧化应激在肿瘤发生过程中起着关键作用，抗氧化剂/氧化剂失衡可能导致正常组织恶性转化。在具有癌症家族易感性的患者中，参与氧化代谢调控的多个基因的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生。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Hereditary Cancer in Clinical Practice 医学-肿瘤学

CiteScore

3.10

自引率

5.90%

发文量

审稿时长

>12 weeks

期刊介绍： Hereditary Cancer in Clinical Practice is an open access journal that publishes articles of interest for the cancer genetics community and serves as a discussion forum for the development appropriate healthcare strategies. Cancer genetics encompasses a wide variety of disciplines and knowledge in the field is rapidly growing, especially as the amount of information linking genetic differences to inherited cancer predispositions continues expanding. With the increased knowledge of genetic variability and how this relates to cancer risk there is a growing demand not only to disseminate this information into clinical practice but also to enable competent debate concerning how such information is managed and what it implies for patient care. Topics covered by the journal include but are not limited to: Original research articles on any aspect of inherited predispositions to cancer. Reviews of inherited cancer predispositions. Application of molecular and cytogenetic analysis to clinical decision making. Clinical aspects of the management of hereditary cancers. Genetic counselling issues associated with cancer genetics. The role of registries in improving health care of patients with an inherited predisposition to cancer.