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

DOI: 10.1186/1756-6614-4-3

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Abstract:

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 ΔΔCT method.COX-2 gene expression was higher in patients with PTC, when compared to specimens from patients with non-toxic nodular goitre (NTG).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.The most common thyroid malignancy is papillary thyroid carcinoma (PTC), accounting for approximately 85-90% of all thyroid cancers. PTC usually grows slowly and is clinically indolent, although aggressive forms can also occur. The 10-year survival rate for all PTC patients is estimated at 80-90% [1].The introduction of fine-needle aspiration biopsy (FNAB) has made PTC identification more accurate, but still the diagnostic tools regarding the differentiation between thyroid benign and malignant lesions are not always reliable. The molecular basis of PTC has been examined and association with variety of molecular prognostic markers has been described, including RAS, RET, Trk, MET, and BRAF mutations [2].Cyclooxygenase-2 (COX-2) is an enzyme isoform involved in the conversion of arachidonic acid to prostaglandin H2, the precursor of various molecules, including prostaglandins, prostacyclines and thromboxanes. COX-2 can be expressed in response to various stimuli, such as hormones, mitogens, cytokines, inflammatory mediators and growth factors via protein kinase C and RAS-mediated signaling [3,4]. The products of COX-2 activity are believed to be involved in carcinogenes

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