A total of 59 PTCs from both groups were evaluated for BRAF mutation on tumor tissue and on ctDNA from plasma samples by real-time polymerase chain reaction (PCR) and digital PCR.
CONCLUSIONS Expression of the BRAFV600E mutation and RET/PTC translocation promoted the activity of NF-κB, expression of inflammatory mediators, and lymph node metastases in patients with PTC.
In the present study, reverse transcription-quantitative polymerase chain reaction was used to determine the expression levels of miR-9-5p and BRAF mRNA in patients with papillary thyroid cancer (PTC).
The aim of the present study was to evaluate the possible diagnostic role of the combined performance of BRAF mutation analysis and MIBI scintigraphy in papillary thyroid cancer (PTC) patients with incomplete bio-chemical response to first radioiodine therapy (RAIT) performed for thyroid remnant ablation.
The B-Raf proto-oncogene serine∕threonine kinase (BRAF) V600E (BRAF(V600E)) mutation represents a very specific marker for papillary thyroid carcinoma (PTC), including microcarcinomas (PTMCs).
Nine thyroid carcinomas with infarction were characterized as BRAF-like papillary thyroid carcinoma based on molecular driver categorization and histologic diagnosis.
However, the mean TIMP3 protein level was significantly lower in tumoral tissues, compared to matched non-tumoral tissues in BRAF (+) PTC (P=0.003); TIMP3 protein level was significantly lower in tumoral tissues compared to matched non-tumoral tissues in BRAF (+), in subjects who had no lymph node metastasis and also in subjects with lymph node metastasis in both BRAF positive and negative PTC cases.
In this study, we used the KTC1 cell line as a model for human advanced papillary thyroid cancer (PTC) because the cells harbor the heterozygous BRAF (V600E) mutation together with the C250T TERT promoter mutation.
We therefore tested TM for antineoplastic activity in <i>BRAF<sup>V600E</sup></i> -positive PTC.<b>Experimental Design:</b> The efficacy of TM alone and in combination with current standard-of-care lenvatinib and sorafenib or BRAF and MEK1/2 inhibitors vemurafenib and trametinib was examined in <i>BRAF<sup>V600</sup></i><sup>E</sup>-positive human PTC cell lines and a genetically engineered mouse PTC model.<b>Results:</b> TM inhibited MEK1/2 kinase activity and transformed growth of PTC cells.