EGFR: The classical anti-tumor drug target epidermal growth factor receptor (EGFR) is the most classic target in the field of anti-tumor, and a variety of drugs based on this target have been marketed. EG

EGFR: Classic antitumor drug target

Epidermal growth factor receptor (EGFR) is the most classic target in the field of anti-tumor, and a variety of drugs based on this target have been marketed. EGFR consists of three parts: extracellular, transmembrane, and intracellular. After EGFR is activated, the downstream signaling pathways undergo cascade reactions, mainly including the following three: EGFR activates Ras/Raf/MEK/ERK1/2 pathway, EGFR-activates JAK/STAT pathway, and EGFR-activates PI3K/Akt pathway. EGFR mutations are the second most common carcinogenic factor in NSCLC, and classical EGFR activating mutations (exon 19 deletion and L858R point mutation) account for 80-90% of the total, which is a strong predictor of good clinical response to EGFR tyrosine kinase inhibitors. Although EGFR tyrosine kinase inhibitors have achieved good clinical results, there are also problems with drug-resistant mutations, such as EGFR T790M mutations, which account for about 50% of all resistance mechanisms.