Progress on the EGFR pathway drives targeted therapy for NSCLC

Abstract

Epidermal growth factor receptor (EGFR) is a key tyrosine kinase receptor that regulates cell survival, proliferation, division, and differentiation. The mutation of the EGFR gene is one of the most common gene mutations responsible for non-small cell lung cancer (NSCLC). Extensive research has been done in the field. Several key EGFR signaling pathways control cell activity, such as MAPK/EPK, PI3K/Akt/mTOR, and JAK/STAT pathways. Mutation of EGFR can cause abnormal activation of signaling cascades, leading to constant cell growth and division, eventually causing tumor growth. Understanding the function of epidermal growth factor receptor and EGFR signaling pathways contributes to the development of targeted treatment for lung cancer. Therefore, through recent research and analysis on the mechanism of action and related pathways of EGFR, this article finds that EGFR tyrosine kinase inhibitor (TKI), a commonly used drug to treat lung cancer, is one of the most effective treatment and it has high potential. However, resistance to TKIs caused by secondary mutations has become a crucial challenge. Novel generations of TKI and combination therapies are needed.