EGFRrelated

EGFRrelated refers to phenomena and research connected with the epidermal growth factor receptor (EGFR), also known as ERBB1. EGFR-related alterations include mutations, amplifications, overexpression, or variant receptors that influence signaling and cellular behavior. EGFR is a transmembrane receptor tyrosine kinase in the ERBB family. It binds ligands such as epidermal growth factor, triggering receptor dimerization, autophosphorylation, and activation of downstream signaling pathways that regulate cell proliferation, survival, differentiation, and migration.

Signal transduction and variation: EGFR signaling proceeds through homo- or heterodimerization with other ERBB family members (ERBB2/HER2, ERBB3, ERBB4). Activated tyrosine residues recruit adaptor proteins that drive pathways including RAS-RAF-MEK-ERK and PI3K-AKT-mTOR, as well as PLCγ and STAT signaling. Regulation is complex and influenced by ligand availability, receptor endocytosis, and cross-talk with other pathways. Mutations or variant forms such as EGFRvIII can alter signaling and drive oncogenic programs, particularly in brain and lung tumors.

Clinical significance: EGFR alterations are common in several cancers. Activating mutations in non-small cell lung cancer predict response to tyrosine kinase inhibitors. EGFR amplification and overexpression occur in glioblastoma and other tumors. Therapies target EGFR with small-molecule inhibitors (gefitinib, erlotinib, afatinib, osimertinib) and monoclonal antibodies (cetuximab, panitumumab). Resistance often develops through secondary mutations, alternative pathway activation, or histologic transformation, necessitating combination strategies or next-generation inhibitors.

Diagnostics and research: EGFR status is assessed by immunohistochemistry, fluorescence in situ hybridization, and sequencing. Beyond oncology, EGFR signaling participates in development, tissue repair, and homeostasis, with dysregulation contributing to skin disorders and neurobiology.