The treatment of different cancers, particularly non-small cell lung cancer (NSCLC), has been transformed by a class of targeted cancer medicines known as epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs). The Epidermal Growth Factor Receptor (EGFR), a cell surface protein that is essential for controlling cell growth and proliferation, is the target of these inhibitors. In some cancer types, EGFR is frequently hyperactive or mutated, which promotes unchecked cell proliferation and tumor growth. The tyrosine kinase activity of the EGFR receptor is blocked by EGFR TKIs. The kinase activity that causes a series of cellular signals to be sent out and encourage cell growth and survival. EGFR TKIs decrease or stop tumor growth by inhibiting this kinase, which interferes with the signaling pathways that promote the growth of cancer cells. First-generation (such as erlotinib and gefitinib), second-generation (such as afatinib), and third-generation (such as osimertinib) EGFR TKIs are some of the EGFR TKIs that are currently on the market. Each generation has unique characteristics and workings. L858R and exon 19 deletions are two prevalent EGFR mutations that are the main targets of first-generation inhibitors. While third-generation inhibitors like osimertinib are developed to tackle resistance mechanisms that develop following therapy with earlier-generation medicines, second-generation inhibitors have a wider range of inhibition. In the treatment of EGFR-mutated NSCLC, EGFR TKIs have demonstrated exceptional effectiveness, frequently leading to considerable tumor reduction and prolonged progression-free survival. However, the emergence of medication resistance, which can be brought on by supplementary mutations in the EGFR gene or the activation of alternative signaling pathways, frequently limits the efficacy of these treatments. In order to overcome resistance and enhance long-term results for patients, ongoing research attempts to create combination therapies and new EGFR TKIs. The negative effects of EGFR TKIs can include skin rash, diarrhea, and gastrointestinal issues despite their great therapeutic benefits. To control adverse effects and improve treatment outcomes, it is crucial to closely monitor patients using these inhibitors. In conclusion, by precisely inhibiting the EGFR signaling pathway, epidermal growth factor receptor tyrosine kinase inhibitors have revolutionized the way that cancer is treated. They have established themselves as a pillar in the treatment of EGFR-mutated NSCLC and show promise in the fight against other malignancies. There is hope for better results and a higher quality of life for cancer patients thanks to ongoing research and development in this area that aims to increase their effectiveness and overcome resistance mechanisms.
