Technical Articles

This article focuses on the molecular structure of the epidermal growth factor receptor (EGFR) protein and the clinical significance of exon 20 mutations, systematically elaborating on the structural organization of the EGFR kinase domain and the conformational change mechanisms underlying exon 20 mutations, analyzing the essential differences in structure-function relationships between exon 20 insertion mutations and point mutations, and exploring the sensitivity patterns of different mutation types to various targeted drugs as well as the corresponding therapeutic strategies.

Murine EGF activates EGFR to drive epithelial proliferation and organoid growth. This article explains the signaling logic and its three research arenas.

In the battlefield of lung cancer treatment, molecular targeted therapy is like a precise "sniper", which brings new hope to patients with its ability to kill tumor cells efficiently and selectively. In particular, targeted drugs targeting epidermal growth factor receptor (EGFR) have become an important part of non-small cell lung cancer (NSCLC) treatment.

EGFR (Epidermal Growth Factor Receptor), also known as ERBB1, is the expression product of the proto-oncogene c-erbB1 and a member of the HER family, which also includes HER2 (erbB2, NEU), HER3 (erbB3), and HER4 (erbB4). These receptors belong to the receptor tyrosine kinase (RTKs) family.