[In these days molecule target drug in advanced non-small cell lung cancer]

Area of Science:

• Oncology
• Molecular Biology
• Pharmacology

Background:

• Conventional chemotherapy (platinum-based, taxanes, gemcitabine, etc.) for advanced non-small cell lung cancer (NSCLC) has reached a plateau in survival benefit.
• Targeted therapies, specifically Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors (EGFR-TKIs) like gefitinib, have emerged as a promising treatment modality for NSCLC.
• Despite initial dramatic responses, acquired resistance to EGFR-TKIs is a significant clinical challenge in NSCLC treatment.

Purpose of the Study:

• To review the clinical trial data on gefitinib for advanced non-small cell lung cancer.
• To explore the role of Epidermal Growth Factor Receptor (EGFR) gene mutations in treatment response and resistance.
• To elucidate the molecular mechanisms underlying acquired resistance to EGFR-TKIs.

Main Methods:

• Review of clinical trial data focusing on gefitinib efficacy in advanced NSCLC.
• Analysis of studies investigating EGFR gene mutations and their correlation with treatment outcomes.
• Examination of research identifying genetic alterations associated with acquired resistance to EGFR-TKIs.

Main Results:

• Gefitinib demonstrates clinical activity in advanced NSCLC, particularly in patients with EGFR mutations.
• EGFR mutations are associated with initial dramatic responses to EGFR-TKIs.
• Acquired resistance to EGFR-TKIs can occur through mechanisms such as the T790M mutation and MET gene amplification.

Conclusions:

• Gefitinib represents a significant advancement in targeted therapy for advanced NSCLC.
• Understanding EGFR mutation status is crucial for patient selection and predicting response to EGFR-TKIs.
• Identifying resistance mechanisms, including T790M and MET amplification, is essential for developing strategies to overcome acquired resistance and improve long-term patient outcomes.