A subset of papillary thyroid carcinomas containKRASmutant subpopulations at levels above normal thyroid

2012 ◽  
Vol 53 (2) ◽  
pp. 159-167 ◽  
Author(s):  
Meagan B. Myers ◽  
Karen L. McKim ◽  
Barbara L. Parsons
2013 ◽  
Vol 38 (2) ◽  
pp. 89-97 ◽  
Author(s):  
Sun Wook Kim ◽  
Hee Kyung Kim ◽  
Ji In Lee ◽  
Hye Won Jang ◽  
Jun-Ho Choe ◽  
...  

1993 ◽  
Vol 107 (12) ◽  
pp. 1174-1176 ◽  
Author(s):  
Kadriye Yildiz ◽  
Haydar Köksal ◽  
Yavuz Özoran ◽  
Hayrettin Muhtar ◽  
Münir Telatar

Carcinoma in the thyroglossal duct remnant is relatively uncommon. Since the first report by Uchermann (1915), more than 150 cases of carcinoma have been reported, and the majority have been papillary thyroid carcinomas (Li Volsi etal., 1974; McNicol etal., 1988). In this report, we present a case of papillary carcinoma in the thyroglossal duct with a normal thyroid gland


2007 ◽  
Vol 92 (7) ◽  
pp. 2840-2843 ◽  
Author(s):  
C. Durante ◽  
E. Puxeddu ◽  
E. Ferretti ◽  
R. Morisi ◽  
S. Moretti ◽  
...  

Abstract Context: BRAF mutations are common in papillary thyroid carcinomas (PTCs). By affecting the expression of genes critically related to the development and differentiation of thyroid cancer, they may influence the prognosis of these tumors. Objective: Our objective was to characterize the expression of thyroid-specific genes associated with BRAF mutation in PTCs. Design/Setting and Patients: We examined the expression of key markers of thyrocyte differentiation in 56 PTCs with BRAF mutations (BRAF-mut) and 37 with wild-type BRAF (BRAF-wt). Eight samples of normal thyroid tissue were analyzed as controls. Quantitative PCR was used to measure mRNA levels for the sodium/iodide symporter (NIS), apical iodide transporter (AIT-B), thyroglobulin (Tg), thyroperoxidase (TPO), TSH receptor (TSH-R), the transcription factor PAX8, and glucose transporter type 1 (Glut1). NIS protein expression and localization was also analyzed by immunohistochemistry. Results: mRNA levels for all thyroid-specific genes were reduced in all PTCs vs. normal thyroid tissues. NIS, AIT-B, Tg, and TPO expression was significantly lower in BRAF-mut tumors than in the BRAF-wt group. Glut-1 transcript levels were increased in all PTCs, and additional increases were noted in BRAF-mut tumors. In both tumor subsets, the NIS protein that was expressed was abnormally retained in the cytoplasm. Conclusion: BRAF V600E mutation in PTCs is associated with reduced expression of key genes involved in iodine metabolism. This effect may alter the effectiveness of diagnostic and/or therapeutic use of radioiodine in BRAF-mut PTCs.


2021 ◽  
Author(s):  
Inês Monteiro ◽  
Edoardo Missiaglia ◽  
Amedeo Sciarra ◽  
João Vasco Santos ◽  
Justine Bouilly ◽  
...  

AbstractCD73 converts AMP to adenosine, an immunosuppressive metabolite that promotes tumorigenesis. This study presents a systematic evaluation of CD73 expression in benign, hyperplastic, and neoplastic thyroid. CD73 expression was assessed by immunohistochemistry in 142 thyroid samples. CD73 was expressed in normal thyroid (3/6) and goiter (5/6), with an apical pattern and mild intensity. Apical and mild CD73 expression was also present in oncocytic cell adenomas/carcinomas (9/10; 5/8) and in follicular adenomas/carcinomas (12/18; 23/27). In contrast, papillary thyroid carcinomas featured extensive and intense CD73 staining (49/50) (vs. normal thyroid/goiter, p < 0.001). Seven of nine anaplastic carcinomas were CD73-positive with heterogeneous extensiveness of staining. Medullary and poorly differentiated carcinomas were mostly CD73-negative (1/6; 2/2). These results were corroborated by NT5E mRNA profiling. Papillary carcinomas feature enhanced CD73 protein and mRNA expression with distinct and intense staining, more pronounced in the invasive fronts of the tumors.


2001 ◽  
Vol 120 (5) ◽  
pp. A507-A507
Author(s):  
M BLAEKER ◽  
A WEERTH ◽  
L JONAS ◽  
M TOMETTEN ◽  
M SCHUTZ ◽  
...  

2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
A Matuszczyk ◽  
S Petersenn ◽  
A Bockisch ◽  
S Sheu ◽  
P Veit ◽  
...  

2019 ◽  
Vol 19 (7) ◽  
pp. 561-570 ◽  
Author(s):  
Hamidreza Maroof ◽  
Soussan Irani ◽  
Armin Arianna ◽  
Jelena Vider ◽  
Vinod Gopalan ◽  
...  

Background: The clinical pathological features, as well as the cellular mechanisms of miR-195, have not been investigated in thyroid carcinoma. Objective: The aim of this study is to identify the interactions of vascular endothelial growth factor (VEGF), p53 and miR-195 in thyroid carcinoma. The clinical and pathological features of miR-195 were also investigated. Methods: The expression levels of miR-195 were identified in 123 primary thyroid carcinomas, 40 lymph nodes with metastatic papillary thyroid carcinomas and seven non-neoplastic thyroid tissues (controls) as well as two thyroid carcinoma cell lines, B-CPAP (from metastasizing human papillary thyroid carcinoma) and MB-1 (from anaplastic thyroid carcinoma), by the real-time polymerase chain reaction. Using Western blot and immunofluorescence, the effects of exogenous miR-195 on VEGF-A and p53 protein expression levels were examined. Then, cell cycle and apoptosis assays were performed to evaluate the roles of miR-195 in cell cycle progression and apoptosis. Results: The expression of miR-195 was downregulated in majority of the papillary thyroid carcinoma tissue as well as in cells. Introduction of exogenous miR-195 resulted in downregulation of VEGF-A and upregulation of p53 protein expressions. Upregulation of miR-195 in thyroid carcinoma cells resulted in cell cycle arrest. Moreover, we demonstrated that miR-195 inhibits cell cycle progression by induction of apoptosis in the thyroid carcinoma cells. Conclusion: Our findings showed for the first time that miR-195 acts as a tumour suppressor and regulates cell cycle progression and apoptosis by targeting VEGF-A and p53 in thyroid carcinoma. The current study exhibited that miR-195 might represent a potential therapeutic target for patients with thyroid carcinomas having aggressive clinical behaviour.


2021 ◽  
Author(s):  
Tomoe Nakao ◽  
Michiko Matsuse ◽  
Vladimir Saenko ◽  
Tatiana Rogounovitch ◽  
Aya Tanaka ◽  
...  

2010 ◽  
Vol 25 (1) ◽  
pp. 38-45 ◽  
Author(s):  
Huasheng Liang ◽  
Yuhua Zhong ◽  
Zuojie Luo ◽  
Yu Huang ◽  
Huade Lin ◽  
...  

Early diagnosis and treatment of thyroid cancers are critical for better prognosis and better survival rates. The purpose of this study was to identify potential diagnostic markers for papillary thyroid carcinomas with distant metastasis. Fifty-eight papillary thyroid tumor specimens (27 papillary thyroid carcinomas with distant metastasis and 31 without metastasis) were examined, and protein expression of pituitary tumor-transforming gene (PTTG), E-cadherin, p27kip1, vascular endothelial growth factor (VEGF)-C, metalloproteinase (MMP) 2, MMP9, chemokine receptor CXCR4, and basic fibroblast growth factor (bFGF) in these tumors was assessed by immunohistochemistry. The clinicopathological variables with diagnostic significance were determined by multivariate analysis, and their diagnostic values were evaluated by ROC curve analysis. PTTG, VEGF-C, MMP2, MMP9, CXCR4, and bFGF were overexpressed in metastatic papillary thyroid carcinomas, whereas p27kip1 expression was elevated only in carcinomas lacking metastasis. Multiple-factor binary ordinal logistic regression analysis revealed that PTTG, VEGF-C, MMP2, and bFGF were independently related to biological metastatic behavior in thyroid tumors, suggesting their potential use as biomarkers. ROC curve analysis showed that among these four proteins, VEGF-C and bFGF were the best diagnostic biomarkers. A VEGF-C and bFGF cluster was the most useful factor for the differential diagnosis between metastatic and non-metastatic papillary thyroid cancers. Thus, the combined use of VEGF-C and bFGF as biomarkers may improve the diagnostic accuracy of papillary thyroid carcinoma and may be useful in multimodal screening programs for the clinical diagnosis of papillary thyroid carcinoma and early detection of papillary thyroid carcinoma with distant metastasis.


Sign in / Sign up

Export Citation Format

Share Document