Head and neck squamous cell carcinoma is quite common in the U.S., covering more than 4% of all cancers each year, and is most susceptible to individuals between 50 and 60 years of age. Squamous cells are a type of epithelial cell that are located all over the body with concentrations in the mouth, throat, neck and cervix. EGFR, or epidermal growth factor receptor, is a trans-membrane glycoprotein that oversees cellular proliferation through its intrinsic tyrosine kinase activity. When EGFR is bound to its ligand, it is phosphorylated by inner tyrosine kinase activity, where downstream pathways are activated and tumors caused by over stimulated cellular proliferation may occur. Because of EGFR’s role in regulating multiple signaling cascades, and for the potential treatment therapies targeted at kinase inhibitor activity, EGFR is of high interest in understanding head and neck squamous cell carcinoma. The following articles used an EGFR antibody in their research.
Simple Western lane view shows lysates of A431 human epithelial carcinoma cell line untreated (-) or treated (+) with 100 ng/mL Recombinant Human EGF (Catalog # 236-EG) for 5 minutes, loaded at 0.2 mg/mL. A specific band was detected for Phospho-EGF R/ErbB1 (Y1086) at approximately 199 kDa (as indicated) using 1:100 dilution of Rabbit Anti-Human Phospho-EGF R/ErbB1 (Y1086) Monoclonal Antibody (Catalog # MAB8967). This experiment was conducted under reducing conditions and using the 12-230 kDa separation system.
Maiti et al used an EGFR antibody to further examine the relationship that SH3GL2 and CDC25A have with the overexpression of EGFR in head and neck squamous cell carcinoma (HNSCC). Previous research shows that 1-7% of HNSCC’s have a mutation in the EGFR gene, and while targeted therapies have been developed, there is more to know regarding its overexpression. First, an EGFR antibody was used on control, dysplastic and HNSCC tissue samples in immunohistochemistry to highlight the molecular differences of EGFR between the three. Their findings suggest that high expression of EGFR is required for the development of the beginning stages of HNSCC. Next, in order to tie the activity of EGFR to either SH3GL2 or CDC25A, the EGFR antibody was used in immunohistochemistry on control epithelium and HNSCC tissue samples. They found that reduced expression of SH3GL2 was correlated with heightened expression of EGFR.
Harari et al also used an EGFR antibody to study different molecular target approaches to treated head and neck squamous cell carcinoma (HNSCC). While Maiti used the EGFR antibody to understand the molecular basis of EGFR over expression in HNSCC, Harari employed the EGFR antibody to find treatments to accompany surgery, radiation and chemotherapy. Because HNSCC cells can become resistant to different treatments, Harari used the EGFR antibody in western blot of HC4 cells. Specifically, the results showed that a combination of 100nm cetuximab and 25nM dasatinib (both EGFR inhibitors) reduce the expression of AKT, MAPK and EGFR. These results suggest that EGFR has a variety of reasons for being a promising molecular target for HNSCC treatment.
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