Co-expression of high levels of β-catenin and EGFR in association with clinicopathological features implicates their clinical utility in risk stratification of PTC patients, and supports the possibility of crosstalk between Wnt/β-catenin and EGFR signaling during PTC progression.
The objective of the present study was to determine the protein expression levels and clinical significance of EHD1, EGFR, caveolin-1 (CAV-1) and RAB11 family interacting protein 3 (RAB11FIP3) in PTC.
In conclusion, high levels of EGFR and its downstream effector, FAK, in association with lymphatic spread and tumour infiltration indicate their involvement in PTC progression and suggest that both molecules may predict its aggressive behaviour.
Concomitant high expression of ERα36, EGFR and HER2 was strongly associated with aggressive behaviors including extrathyroidal extension (ETE), lymph node metastasis (LNM) and high TNM stage in PTCs (P < 0.001).
We report the case of an 80-year-old woman who had a papillary thyroid carcinoma with a v-raf murine sarcoma viral oncogene homologue B1 mutation that metastasized into a lung adenocarcinoma with an epidermal growth factor receptor mutation.
Low Mig-6 expression in PTC specimens was associated with low NF-κB activity but high levels of epidermal growth factor receptor (EGFR) and ERK phosphorylation.
Our data suggest that EGFR-tyrosine-kinase inhibitors may deserve consideration in the treatment of a subset of patients with PTC, just as with pulmonary adenocarcinoma.
To clarify the significance of KIT, EGFR, and HER-2 in undifferentiated thyroid carcinoma (UTC), the expression of these receptors and tyrosine phosphorylation was examined immunohistochemically in resected cases of UTC and papillary thyroid carcinoma (PTC).
We have found that TGF-alpha and EGF-R/c-erbB RNAs were co-expressed at significantly higher levels in papillary thyroid carcinomas and their lymph-node metastases than in non-neoplastic thyroid tissues.