In vitro iodide uptake studies in SW1736 and Hth74 ATC cells, and, for comparison, in more differentiated follicular (FTC-133) and papillary (BCPAP) thyroid carcinoma cells demonstrated high transfection efficiency and EGFR-specificity of LPEI-PEG-GE11/NIS that correlated well with EGFR expression levels.
Therefore, future investigations of EGFR should consider histologic and immunohistochemical methods, in addition to molecular profiling of thyroid carcinomas.
We, therefore, provide a mechanistic link between the miR-200 family and EGF/EGFR, which suggests that miR-200 upregulation may serve as a novel therapeutic strategy for highly invasive thyroid cancers.
Mig-6 knockdown in thyroid cancer cell lines resulted in EGFR phosphorylation and diminished NF-κB activity, whereas Mig-6 overexpression had the opposite effects.
There are no quantitative data on the mRNA expression of epidermal growth factor receptor (EGFR) and transformation growth factor alpha (TGF-α) in thyroid carcinoma.
Furthermore, PTC clinical samples analyzed by real-time RT-PCR expressed EGFR transcript levels similar to those of 5 normal thyroid tissues from patients with pathologies other than thyroid cancer, whereas significantly elevated levels of TGFA transcripts were only present in PTCs.
The therapeutic role of EGFR inhibitors in thyroid malignancies is still controversial even though the full activation of EGF signaling has recently been proposed as involved in the dedifferentiation of human thyroid cancers.
Targeting epidermal growth factor receptor 1 signaling in human thyroid-stimulating hormone-independent thyroid carcinoma FRO cells results in a more chemosensitive and less angiogenic phenotype.
In this study we evaluate the association of two single-nucleotide polymorphisms (SNP), R497K and I655V, of the EGFR and HER2 genes, respectively, with thyroid cancer risk.
We hypothesized that signaling via the epidermal growth factor receptor (EGFR) stimulates thyroid cancer cell invasion by altering the expression and cleavage of matrix metalloproteinases (MMPs).
The presence of EGFR-activating TK domain mutations may identify a small minority of thyroid cancer patients that may benefit from EGFR inhibitors, but additional preclinical evidence of efficacy is needed.
Epidermal growth factor receptor and ephrin B2 mRNA expression was elevated in higher TNM stage neoplasms and in patients with high-risk AMES (Age, distant Metastasis, Extrathyroidal invasion, and tumor Size) differentiated thyroid cancers (P < or = .005).