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Korean J Endocr Surg. 2002 Dec;2(2):90-96. Korean. Original Article. https://doi.org/10.16956/kjes.2002.2.2.90
Lee KJ , Park HB , Kim JH , Jeong YS , Joo HJ , Soh EY .
Department of Surgery, Ajou University School of Medicine, Suwon, Korea. sohey@ajou.ac.kr
Department of Pathology, Ajou University School of Medicine, Suwon, Korea.
Abstract

PURPOSE: Thyroid tumor is one of the most common endocrine tumors, and yet little is known about its molecular process of development and progression. Cyclooxygenase (COX)-2, the inducible form of the COX enzyme for prostaglandin synthesis, is up-regulated in gastrointestinal cancers and is a key mediator of epithelial cell growth. Regular intake of aspirin or other nonsteroidal antiinflammatory drugs (NSAIDs) is associated with a decreased incidence of colorectal, esophageal, gastric, and lung cancer. We sought to determine the involvement of COX-2 in human thyroid cancer. METHODS: COX-2 protein was assayed in thyroid tissue of 64 which were inflammatory disease and benign tumor and malignant tumor with or without metastasis patients by using immunohistochemistry and Western Blot analysis. RESULTS: COX-2 protein was not expressed in normal thyroid tissue. But COX-2 protein was expressed strongly in inflammatory tissue. Expression of COX-2 was very high in both benign and malignant tumor. There is no difference in pathology and malignant potential or existence of metastasis. CONCLUSION: There was no correlation between clinicopathological characteristics of thyroid tumor and intensity of COX-2 protein expression. In addition, there was no difference of expression of COX-2 between inflammatory thyroid disease and thyroid tumor. This study indicates that COX-2 protein over expression may contribute to an early event of gastric cancer development, and it further suggests that selective inhibition of COX-2 may provide a chemopreventive effect against thyroid cancer.

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