{"title":"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。","authors":"Ivane Javakhishvili, Kote Mardaleishvili, Maka Buleishvili, Maia Mantskava, Irakli Chkhikvishvili, Sophio Kalmakhelidze, Nina Kipiani, Tamar Sanikidze","doi":"10.1186/s13053-024-00287-3","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Aim: </strong>Identification of the possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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<sub>1,2</sub>=0.5, p<sub>1,2</sub>=0.8, F<sub>1,3</sub>=2.31, p<sub>1,3</sub>=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<sub>1,2</sub>=107, p<sub>1,2</sub><0.001), Group 3-2.47 ± 0.17 (F<sub>1,3</sub>=150, p<sub>1,3</sub><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<sub>1 - 2</sub>=200; p<sub>1 - 2</sub><0.001), in patients without genetic predisposition to cancer(Group 3), the level of TAA did not change compared to the control (F<sub>1 - 3</sub>= 2.13; p<sub>1 - 3</sub>=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.</p>","PeriodicalId":55058,"journal":{"name":"Hereditary Cancer in Clinical Practice","volume":"22 1","pages":"15"},"PeriodicalIF":2.0000,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11342469/pdf/","citationCount":"0","resultStr":"{\"title\":\"Possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.\",\"authors\":\"Ivane Javakhishvili, Kote Mardaleishvili, Maka Buleishvili, Maia Mantskava, Irakli Chkhikvishvili, Sophio Kalmakhelidze, Nina Kipiani, Tamar Sanikidze\",\"doi\":\"10.1186/s13053-024-00287-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Aim: </strong>Identification of the possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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<sub>1,2</sub>=0.5, p<sub>1,2</sub>=0.8, F<sub>1,3</sub>=2.31, p<sub>1,3</sub>=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<sub>1,2</sub>=107, p<sub>1,2</sub><0.001), Group 3-2.47 ± 0.17 (F<sub>1,3</sub>=150, p<sub>1,3</sub><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<sub>1 - 2</sub>=200; p<sub>1 - 2</sub><0.001), in patients without genetic predisposition to cancer(Group 3), the level of TAA did not change compared to the control (F<sub>1 - 3</sub>= 2.13; p<sub>1 - 3</sub>=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.</p>\",\"PeriodicalId\":55058,\"journal\":{\"name\":\"Hereditary Cancer in Clinical Practice\",\"volume\":\"22 1\",\"pages\":\"15\"},\"PeriodicalIF\":2.0000,\"publicationDate\":\"2024-08-23\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11342469/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Hereditary Cancer in Clinical Practice\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s13053-024-00287-3\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Hereditary Cancer in Clinical Practice","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s13053-024-00287-3","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
Possible link between familial susceptibility to cancer and the level of oxidative stress in thyroid cancer patients.
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 (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.
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.
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