EGFR mutations in lung cancer: Implications for personalized therapy

Abstract

Author(s): Suphiya Parveen, Krishan Kumar, Praveen Mathur

Objective: The Epidermal Growth Factor Receptor (EGFR) is mutated in 15% of lung adenocarcinomas. Eight percent of instances with altered Anaplastic Lymphoma Kinase (ALK) are caused by lung adenocarcinomas. For tumours of Non-Small Cell Lung Cancer (NSCLC) that are EGFR mutant and ALK translocation positive, Tyrosine Kinase Inhibitor therapy (TKI therapy) has changed treatment and produced a remarkable preventive effect. Unfortunately, TKI resistance always appears to spread. To overcome the resistance, numerous innovative and promising medicines are being studied.

Results: First-line, recognized opposition, and adjuvant treatment is being investigated for NSCLC with EGFR mutation and ALK positivity, along with the therapeutic implications of recent national meetings and beginning research.

Conclusion: There is a signi icant therapeutic advantage to including EGFR TKIs in EGFR mutant NSCLC First Line (FL) therapy. In phase II and III studies, several possible third-generation EGFR TKIs are being examined in the context of acquired resistance. The medicine is better than chemotherapy as an FL treatment for NSCLC with ALK positivity. For NSCLC with established resistance and an ALK-positive test result, cetinib is approved and effective. More study is needed to develop new medications that can combat acquired resistance to TKIs.

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