EGFR in Oncology: A Narrative Review of Mutations, Overexpression and Treatment Strategies

Abstract

The epidermal growth factor receptor (EGFR) was the first member of a broad family of growth factor receptors with intrinsic tyrosine kinase activity. While lung cancer commonly exhibits point mutations and minor insertions within the kinase domain, brain tumours typically exhibit high abundance of EGFR and massive internal deletions. These factors led to the widespread use of EGFR and HER2/ERBB2 as targets for anti-cancer treatments. The association between EGFR expression and cancer prognosis is investigated in this review paper. EGFR, when activated by a ligand, starts a sequence of time-dependent molecular switches that govern genes that determine phenotype. These switches include up-regulation of freshly synthesised mRNAs, down-regulation of a large cohort of microRNAs, and covalent protein changes. Long non-coding RNAs and circular RNAs, in addition to microRNAs, are essential for EGFR signalling. EGFR is a multifaceted driver of metastasis, in addition to driver mutations. Targeted therapies against EGFR, including tyrosine kinase inhibitors and monoclonal antibodies, have significantly improved treatment outcomes in cancers such as non-small cell lung cancer and colorectal cancer. In this review, we discussed about how EGFR overexpression and mutations affect different types of human malignancies. Finally, we evaluated all anti-cancer medications that have received clinical approval that target EGFR and discuss recent advancements in therapy as well as in future possibilities.