Decrease in thyroid adenoma associated (THADA) expression is a marker of dedifferentiation of thyroid tissue

نویسندگان

  • Lars Kloth
  • Gazanfer Belge
  • Käte Burchardt
  • Siegfried Loeschke
  • Werner Wosniok
  • Xin Fu
  • Rolf Nimzyk
  • Salah A Mohamed
  • Norbert Drieschner
  • Volkhard Rippe
  • Jörn Bullerdiek
چکیده

BACKGROUND Thyroid adenoma associated (THADA) has been identified as the target gene affected by chromosome 2p21 translocations in thyroid adenomas, but the role of THADA in the thyroid is still elusive. The aim of this study was to quantify THADA gene expression in normal tissues and in thyroid hyper- and neoplasias, using real-time PCR. METHODS For the analysis THADA and 18S rRNA gene expression assays were performed on 34 normal tissue samples, including thyroid, salivary gland, heart, endometrium, myometrium, lung, blood, and adipose tissue as well as on 85 thyroid hyper- and neoplasias, including three adenomas with a 2p21 translocation. In addition, NIS (sodium-iodide symporter) gene expression was measured on 34 of the pathological thyroid samples. RESULTS Results illustrated that THADA expression in normal thyroid tissue was significantly higher (p < 0.0001, exact Wilcoxon test) than in the other tissues. Significant differences were also found between non-malignant pathological thyroid samples (goiters and adenomas) and malignant tumors (p < 0.001, Wilcoxon test, t approximation), anaplastic carcinomas (ATCs) and all other samples and also between ATCs and all other malignant tumors (p < 0.05, Wilcoxon test, t approximation). Furthermore, in thyroid tumors THADA mRNA expression was found to be inversely correlated with HMGA2 mRNA. HMGA2 expression was recently identified as a marker revealing malignant transformation of thyroid follicular tumors. A correlation between THADA and NIS has also been found in thyroid normal tissue and malignant tumors. CONCLUSIONS The results suggest THADA being a marker of dedifferentiation of thyroid tissue.

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عنوان ژورنال:

دوره 11  شماره 

صفحات  -

تاریخ انتشار 2011