Epidermal growth factor receptor tyrosine kinase inhibitor remodels tumor microenvironment by upregulating LAG-3 in advanced non-small-cell lung cancer

Immune checkpoint inhibitors (ICIs) targeting programmed death 1 (PD-1) and its ligand (PD-L1), which elicit durable clinical responses, have drastically revolutionized treatment patterns in non-small-cell lung cancer (NSCLC) [1 –3]. Preclinical studies have proved that a mutant epidermal growth factor receptor (EGFR) gene could upregulate tumor PD-L1 expression through signal pathways such as PI3K-AKT-mTOR, Hippo-YAP and IL6-JAK-STAT3, theoretically supporting the use of PD-1/PD-L1 inhibitors in NSCLC patients having EGF R mutations [4–6].
Source: Lung Cancer - Category: Cancer & Oncology Authors: Source Type: research