Several driver mutations have been identified in Non-Small Cell Lung Cancer, such as epidermal growth factor receptor (EGFR) mutations, anaplastic lymphoma kinase (ALK) rearrangements, ROS1 rearrangements, and BRAF mutations. These alterations serve as targets for specific molecularly targeted therapies. For example, EGFR-mutated NSCLC patients can be treated with EGFR tyrosine kinase inhibitors (TKIs) like gefitinib, erlotinib, or osimertinib, which specifically inhibit the activity of mutated EGFR and block downstream signaling pathways. Similarly, ALK or ROS1 rearrangements can be targeted with ALK or ROS1 inhibitors, respectively.
In addition to driver mutations, precision medicine also considers other molecular characteristics of Non-Small Cell Lung Cancer tumors, such as tumor mutational burden (TMB) and programmed death-ligand 1 (PD-L1) expression. TMB refers to the number of somatic mutations present in the tumor genome and is indicative of the overall mutation rate. High TMB has been associated with increased response to immune checkpoint inhibitors, which block the interaction between PD-1 and PD-L1, unleashing the immune system to attack cancer cells. PD-L1 expression levels on tumor cells can help predict response to immune checkpoint inhibitors, with higher expression correlating with improved outcomes.
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