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

Krawczyk-Rusiecka K, Wojciechowska-Durczyńska K, Cyniak-Magierska A, Adamczewski Z, Gałecka E, Lewiński A - Thyroid Res (2011)

Bottom Line: Suppressed angiogenesis was found in experimental animal studies as a consequence of mutation of COX-2 gene in mice.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Polish Mother's Memorial Hospital - Research Institute, Lodz, Poland. alewin@csk.umed.lodz.pl.

ABSTRACT

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 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 ΔΔCT 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.

No MeSH data available.


Related in: MedlinePlus

Representative amplification curves for COX-2 and β-actin genes in real-time PCR in macroscopically unchanged specimen. 1 a,b,c - amplification curve for COX-2 gene (mean CT value - 31.979); 2 - amplification curve for β-actin gene (endogenous control) (mean CT value - 27.250).
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Figure 2: Representative amplification curves for COX-2 and β-actin genes in real-time PCR in macroscopically unchanged specimen. 1 a,b,c - amplification curve for COX-2 gene (mean CT value - 31.979); 2 - amplification curve for β-actin gene (endogenous control) (mean CT value - 27.250).

Mentions: COX-2 mRNA expression was significantly higher in PTC when compared to benign thyroid lesions (Student's t-test, P = 0.021). There was no significant relationship between COX-2 expression and patients age and sex. The amplification plots of COX-2 and β-actin are shown in Figure. 1 and 2. The statistical analysis of COX-2 expression by quantitative Real Time PCR in PTC and NTG is presented in Figure. 3 and Figure. 4.


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

Krawczyk-Rusiecka K, Wojciechowska-Durczyńska K, Cyniak-Magierska A, Adamczewski Z, Gałecka E, Lewiński A - Thyroid Res (2011)

Representative amplification curves for COX-2 and β-actin genes in real-time PCR in macroscopically unchanged specimen. 1 a,b,c - amplification curve for COX-2 gene (mean CT value - 31.979); 2 - amplification curve for β-actin gene (endogenous control) (mean CT value - 27.250).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3025973&req=5

Figure 2: Representative amplification curves for COX-2 and β-actin genes in real-time PCR in macroscopically unchanged specimen. 1 a,b,c - amplification curve for COX-2 gene (mean CT value - 31.979); 2 - amplification curve for β-actin gene (endogenous control) (mean CT value - 27.250).
Mentions: COX-2 mRNA expression was significantly higher in PTC when compared to benign thyroid lesions (Student's t-test, P = 0.021). There was no significant relationship between COX-2 expression and patients age and sex. The amplification plots of COX-2 and β-actin are shown in Figure. 1 and 2. The statistical analysis of COX-2 expression by quantitative Real Time PCR in PTC and NTG is presented in Figure. 3 and Figure. 4.

Bottom Line: Suppressed angiogenesis was found in experimental animal studies as a consequence of mutation of COX-2 gene in mice.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.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Endocrinology and Metabolic Diseases, Medical University of Lodz, Polish Mother's Memorial Hospital - Research Institute, Lodz, Poland. alewin@csk.umed.lodz.pl.

ABSTRACT

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 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 ΔΔCT 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.

No MeSH data available.


Related in: MedlinePlus