High IL-17 expression is associated with an unfavorable prognosis in thyroid cancer

Previous studies have indicated that cancer may be promoted and/or exacerbated by inflammation and infection. The cytokines produced by activated innate immune cells that stimulate tumor growth and progression are considered as important components in this process. The interleukin (IL)-23/T helper (...

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Published in:Oncology letters Vol. 13; no. 3; pp. 1925 - 1931
Main Authors: Carvalho, Denise Faria Galano, Zanetti, Bruna Riedo, Miranda, Lydianne, Hassumi-Fukasawa, Marcela Kazue, Miranda-Camargo, Fabiana, Crispim, Janaína Cristiana Oliveira, Soares, Edson Garcia
Format: Journal Article
Language:English
Published: Greece Spandidos Publications 01-03-2017
Spandidos Publications UK Ltd
D.A. Spandidos
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Summary:Previous studies have indicated that cancer may be promoted and/or exacerbated by inflammation and infection. The cytokines produced by activated innate immune cells that stimulate tumor growth and progression are considered as important components in this process. The interleukin (IL)-23/T helper (Th)17 axis, which exerts marked pro-inflammatory effects, has emerged as an important mediator in inflammation-associated cancer. Increasing clinical evidence indicates that Th17 may promote or inhibit tumor progression, however, the function of Th17 in the pathogenesis of benign and malignant thyroid neoplasms remains unclear. The present study investigated the association between the IL-23/Th17 axis and neoplastic and non-neoplastic thyroid lesions using immunohistochemistry. A total of 131 thyroid biopsy specimens were analyzed, which revealed high IL-17 and IL-23 expression in differentiated thyroid cancer and medullary thyroid cancer tissues when compared with benign lesions, including follicular thyroid adenoma and goiter tissues. Furthermore, high IL-17 expression was associated with recurrence and mortality. These results indicate that the IL-23/Th17 axis exhibits a pivotal function in the development of thyroid neoplasms.
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ISSN:1792-1074
1792-1082
DOI:10.3892/ol.2017.5638