Epidermal growth factor receptor (mutant) (EGFR (mutant))

The **mutant epidermal growth factor receptor** is a transmembrane receptor tyrosine kinase belonging to the ErbB (HER) family, whose gene (EGFR) is frequently mutated in human cancers, notably non-small cell lung cancer[2][4][6][8]. Common mutations—such as exon 19 deletions, L858R substitution in exon 21, and various insertions or point mutations—result in constitutive activation of the receptor's kinase domain, driving uncontrolled cell proliferation and survival[4][5][6]. EGFR mutations confer sensitivity to various targeted therapies, notably tyrosine kinase inhibitors (TKIs) like osimertinib, gefitinib, and erlotinib, although secondary resistance mutations (e.g., T790M) often develop, affecting long-term efficacy[1][4]. Mutant EGFR status guides treatment selection and predicts response, and is therefore employed as both a therapeutic target and a predictive biomarker in oncology practice[3][5]. The receptor's pivotal role in signaling pathways critical for cell growth and survival, as well as its frequent alteration in diverse cancers, have established it as a major therapeutic target[2][4][6][8].

Other names

EGFR (mutant)Mutant EGFRMutated epidermal growth factor receptorMutant ErbB1 receptorMutant HER1

Tyrosine kinase inhibition (EGFR-TKIs): block ATP binding in the kinase domain, inhibiting phosphorylation and downstream signaling[2][4][5]. Monoclonal antibody blockade: block ligand binding and receptor activation[2][6][8]. Dual targeting (antibody/EGFR+MET inhibition): some agents target EGFR and other pathways[5].