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Background  COX-2 is an enzyme isoform that catalyses the formation of prostanoids from arachidonic acid. An increased  COX-2  gene expression is believed to participate in carcinogenesis. Recent studies have shown that  COX-2  up-regulation is associated with the development of numerous neoplasms, including skin, colorectal, breast, lung, stomach, pancreas and liver cancers.  COX-2  products stimulate endothelial cell proliferation and their overexpression has been demonstrated to be involved in the mechanism of decreased resistance to apoptosis. Suppressed angiogenesis was found in experimental animal studies as a consequence of null mutation of  COX-2  gene in mice. Despite the role of  COX-2  expression remains a subject of numerous studies, its participation in carcinogenesis or the thyroid cancer progression remains unclear.    Methods  Twenty three (23) patients with cytological diagnosis of PTC were evaluated. After FNAB examination, the needle was washed out with a lysis buffer and the obtained material was used for  COX-2  expression estimation. Total RNA was isolated (RNeasy Micro Kit), and RT reactions were performed. β-actin was used as endogenous control. Relative  COX-2  expression was assessed in real-time PCR reactions by an ABI PRISM 7500 Sequence Detection System, using the ΔΔC T  method.    Results   COX-2  gene expression was higher in patients with PTC, when compared to specimens from patients with non-toxic nodular goitre (NTG).    Conclusions  The preliminary results may indicate  COX-2  role in thyroid cancer pathogenesis, however the observed variability in results among particular subjects requires additional clinical data and tumor progression analysis.

COX-2 expression in papillary thyroid carcinoma (PTC) in cytological material obtained by fine needle aspiration biopsy (FNAB)