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About this Research Topic

Manuscript Submission Deadline 20 November 2022
Manuscript Extension Submission Deadline 18 December 2022

Epidermal Growth Factor Receptor (EGFR) is a member of the ErbB family of the receptor tyrosine kinases, in which its upregulation is found in various types of cancers. The EGFR overexpression consequently activates prooncogenic downstream signaling pathways including RAS/RAF/MEK/ERK and PI3K/AKT/mTOR, which ...

Epidermal Growth Factor Receptor (EGFR) is a member of the ErbB family of the receptor tyrosine kinases, in which its upregulation is found in various types of cancers. The EGFR overexpression consequently activates prooncogenic downstream signaling pathways including RAS/RAF/MEK/ERK and PI3K/AKT/mTOR, which are involved in cell survival, cell proliferation, cell differentiation, apoptosis evasion, and metastasis. Accordingly, the EGFR is considered one of the attractive targets for cancer treatment. The first-generation tyrosine kinase inhibitors (i.e., erlotinib and gefitinib) were developed as reversible EGFR inhibitors. However, these drugs are concerned for their acquired drug resistance (caused by T790M and C797S mutations) and considerable side effects. Therefore, the discovery of novel EGFR inhibitors with minimized toxicity is needed.

This Research Topic will showcase the recent trends in the field of drug discovery of EGFR tyrosine kinase inhibitors.

We welcome Original Research, Review, Mini Review, and Perspective articles on themes including, but not limited to:

• Mechanistic insight of naturally occurring small molecules and their semisynthetic derivatives against EGFR tyrosine kinase (wild-type, L858R/T790M, and L858R/T790M/C797S forms).

• A broad range of in silico methods from molecular modeling to artificial intelligence to discover novel EGFR inhibitors

• Drug repurposing strategy to identify novel EGFR inhibitors

• Anticancer and its underlying mechanisms of natural products/synthetic compounds against cancer cells overexpressing EGFR.

• Molecular interactions of small-molecule inhibitors against wild-type, L858R/T790M, and L858R/T790M/C797S forms of EGFR

• Drug combination to target EGFR signaling pathways

Keywords: EGFR inhibitors, Medicinal chemistry, Cancer, Repurposing approach, Molecular biology, Drug Discovery, Anti-Cancer Drugs


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