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      Clinical significance of oxidative stress markers as angioinvasion and metastasis indicators in papillary thyroid cancer

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          Abstract

          Angioinvasion remains the important prognostic feature in papillary thyroid cancer (PTC) patients. Literature data indicates several markers that may be associated with oxidative stress and/or angioinvasion. Therefore, we assessed the utility of selected parameters in angioinvasion and metastasis screening in serum of PTC patients. Serum antioxidant capacity (TAC) and sirtuin 3 (SIRT3) levels were decreased (all p < 0.05) and both DNA/RNA oxidative stress damage products (DNA/RNA OSDP) and malondialdehyde (MDA) levels were increased in PTC patients with angioinvasion and metastasis (study group) when compared with PTC patients without these features (all p < 0.01). The highest screening utility in differentiation between angioinvasion and metastasis presence and absence in PTC patients was presented for DNA/RNA OSDP (AUC = 0.71), SIRT3 (AUC = 0.70), and TAC (AUC = 0.67) (all p < 0.05). Our study suggests that peripheral concentration of oxidative stress markers could be useful as angioinvasion and metastasis indicator in PTC patients.

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          Most cited references47

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          2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer.

          Thyroid nodules are a common clinical problem, and differentiated thyroid cancer is becoming increasingly prevalent. Since the American Thyroid Association's (ATA's) guidelines for the management of these disorders were revised in 2009, significant scientific advances have occurred in the field. The aim of these guidelines is to inform clinicians, patients, researchers, and health policy makers on published evidence relating to the diagnosis and management of thyroid nodules and differentiated thyroid cancer.
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            Oxidative stress, inflammation, and cancer: how are they linked?

            Extensive research during the past 2 decades has revealed the mechanism by which continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer, diabetes, and cardiovascular, neurological, and pulmonary diseases. Oxidative stress can activate a variety of transcription factors including NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. Activation of these transcription factors can lead to the expression of over 500 different genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. How oxidative stress activates inflammatory pathways leading to transformation of a normal cell to tumor cell, tumor cell survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival is the focus of this review. Overall, observations to date suggest that oxidative stress, chronic inflammation, and cancer are closely linked. Copyright © 2010 Elsevier Inc. All rights reserved.
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              Oxidative Stress in Cancer

              Contingent upon concentration, reactive oxygen species (ROS) influence cancer evolution in apparently contradictory ways, either initiating/stimulating tumorigenesis and supporting transformation/proliferation of cancer cells or causing cell death. To accommodate high ROS levels, tumor cells modify sulfur-based metabolism, NADPH generation, and the activity of antioxidant transcription factors. During initiation, genetic changes enable cell survival under high ROS levels by activating antioxidant transcription factors or increasing NADPH via the pentose phosphate pathway (PPP). During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.
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                Author and article information

                Contributors
                angelika.buczynska@umb.edu.pl
                annapoplawskakita@op.pl
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                22 August 2023
                22 August 2023
                2023
                : 13
                : 13711
                Affiliations
                [1 ]GRID grid.48324.39, ISNI 0000000122482838, Clinical Research Centre, , Medical University of Bialystok, ; 15-276 Białystok, Poland
                [2 ]GRID grid.48324.39, ISNI 0000000122482838, Clinical Research Support Centre, , Medical University of Bialystok, ; Ul. M. Skłodowskiej-Curie 24a, 15-276 Białystok, Poland
                [3 ]GRID grid.48324.39, ISNI 0000000122482838, Department of Endocrinology, Diabetology and Internal Medicine, , Medical University of Bialystok, ; 15-276 Białystok, Poland
                [4 ]GRID grid.48324.39, ISNI 0000000122482838, Department of Human Anatomy, , Medical University of Bialystok, ; 15-276 Białystok, Poland
                [5 ]GRID grid.48324.39, ISNI 0000000122482838, Nuclear Medicine, , Medical University of Bialystok, ; 15-276 Białystok, Poland
                Article
                40898
                10.1038/s41598-023-40898-9
                10444813
                37608150
                ce145bc9-315d-425e-b93f-581b64a603da
                © Springer Nature Limited 2023

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 6 April 2023
                : 17 August 2023
                Funding
                Funded by: internal financing of Medical University of Bialystok
                Award ID: SUB/1/DN/22/002/1150
                Award Recipient :
                Categories
                Article
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                © Springer Nature Limited 2023

                Uncategorized
                thyroid cancer,cancer screening
                Uncategorized
                thyroid cancer, cancer screening

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