scholarly journals Current Status of Anti Epidermal Growth Factor Receptor Therapy in the Curative Treatment of Head and Neck Squamous Cell Carcinoma

2017 ◽  
Vol 3 (1) ◽  
pp. 1-6
Author(s):  
Cessal Thommachan Kainickal ◽  
◽  
Aparna M. P. ◽  
Rejnish Kumar Ravi Kumar ◽  
Malu Rafi ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Growth Factor Receptor ◽  
Current Status ◽  
Epidermal Growth

scholarly journals Honokiol inhibits the growth of head and neck squamous cell carcinoma by targeting epidermal growth factor receptor

Oncotarget ◽  
2015 ◽  
Vol 6 (25) ◽  
pp. 21268-21282 ◽  
Author(s):  
Tripti Singh ◽  
Nirzari A. Gupta ◽  
Su Xu ◽  
Ram Prasad ◽  
Sadanandan E. Velu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Growth Factor Receptor ◽  
Neck Squamous Cell Carcinoma ◽  
Epidermal Growth

scholarly journals Preferential Response of Basal-Like Head and Neck Squamous Cell Carcinoma Cell Lines to EGFR-Targeted Therapy Depending on EREG-Driven Oncogenic Addiction

Cancers ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 795 ◽  
Author(s):  
Sylvie Job ◽  
Aurélien de Reyniès ◽  
Betty Heller ◽  
Amélie Weiss ◽  
Eric Guérin ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Cell Lines ◽  
Squamous Cell ◽  
Growth Factor Receptor ◽  
Epidermal Growth

The management of locally advanced head and neck squamous cell carcinoma (HNSCC) with Cetuximab, a monoclonal antibody targeting the epidermal growth factor receptor (EGFR), achieves only moderate response rates, and clinical trials that evaluated EGFR-blockade with tyrosine kinase inhibitors (TKI) yielded disappointing results. Inter-tumor heterogeneity may hinder the therapeutic efficiency of anti-EGFR treatments. HNSCC heterogeneity was addressed in several studies, which all converged towards the definition of molecular subgroups. They include the basal subgroup, defined by the deregulated expression of factors involved in the EGFR signaling pathway, including the epiregulin EGFR ligand encoded by the EREG gene. These observations indicate that basal tumors could be more sensitive to anti-EGFR treatments. To test this hypothesis, we performed a screen of a representative collection of basal versus non-basal HNSCC cell lines for their sensitivity to several anti-EGFR drugs (Cetuximab, Afatinib, and Gefitinib), tested as monotherapy or in combination with drugs that target closely-linked pathways [Mitogen-activated protein kinase kinase/extracellular signal–regulated kinases (MEK), mammalian Target of Rapamycine (mTOR) or Human Epidermal growth factor Receptor 2 (HER2)]. Basal-like cell lines were found to be more sensitive to EGFR blockade alone or in combination with treatments that target MEK, mTOR, or HER2. Strikingly, the basal-like status was found to be a better predictor of cell response to EGFR blockade than clinically relevant mutations [e.g., cyclin-dependent kinase Inhibitor 2A (CDKN2A)]. Interestingly, we show that EGFR blockade inhibits EREG expression, and that EREG knock-down decreases basal cell clonogenic survival, suggesting that EREG expression could be a predictive functional marker of sensitivity to EGFR blockade in basal-like HNSCC.

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