Blocking EGFR signaling caused HGF-induced squamous tumors to regress, suggesting that EGFR inhibitors might be useful for treating squamous cell carcinomas.Listen to Podcast.
Genomic gain of the epidermal growth factor receptor harboring band 7p12 is part of a complex pattern of genomic imbalances in oral squamous cell carcinomas.
We found EGFR expression is higher in the squamous cell carcinomas than in adenocarcinomas (p=0.043), and that nuclear p53 staining correlated with lower differentiated squamous tumors (p=0.034).
Transforming growth factor alpha (TGF-alpha) and epidermal growth factor receptor (EGFR) have been shown to be present in most squamous cell carcinomas.
However, an adjacent gene (approximately 0.4 Mb), EGFR-co-amplified and overexpressed protein (ECOP), showed strong over-expression in the majority (90%) of SCCs regardless of gene amplification status.
EGFR gene copy number was positively correlated with EGFR protein expression among both AD samples (P=0.008) and SCC samples (P=0.042), with EGFR protein expression being significantly higher in SCC samples compared with AD (P=0.038).
The balance between 4-hydroxynonenal and intrinsic glutathione/glutathione S-transferase A4 system may be critical for the epidermal growth factor receptor phosphorylation of human esophageal squamous cell carcinomas.
The anti-human epidermal growth factor receptor IgG conjugated to ZZ-BNC (α-hEGFR-ZZ-BNC) was endocytosed by the human epidermoid carcinoma A431 cells, with increases in cellular uptake by ∼1.5 fold, compared that of α-hEGFR IgG alone.
Increased expression of the epidermal growth factor receptor has been noted in many types of tumors and is associated with gene amplification in several including epidermoid carcinoma, lung carcinoma, breast carcinoma and glioblastoma.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the EGFR with high specificity and have been developed as promising therapeutic anticancer treatments in several solid tumors, including colorectal and head and neck squamous cell carcinomas.
HR-HPV positivity is associated with decreased expression of the p53 and Rb genes, overexpression of p16, decreased expression of EGFR, and a different genetic expression pattern compared with patients with HR-HPV-negative SCCAs, leading to the conclusion that this is a distinct clinical entity.
Together, our findings provide evidence that ΔNp63α expression is regulated by EGFR activation through STAT3 and that the EGFR-ΔNp63α axis is crucial for proliferation of TICs present in SCCs.