EGFR mutant lung cancer.

Gong Y, Pao W
Curr Top Microbiol Immunol. 2012 355: 59-81

PMID: 21866438 · DOI:10.1007/82_2011_171

Thoracic oncologists traditionally have made treatment decisions based upon tumor histology, distinguishing non-small cell lung cancer (NSCLC) from small cell lung cancer (SCLC). However, recent data has revealed that at least one histological subtype of NSCLC, lung adenocarcinoma comprises multiple molecularly distinct diseases. Lung adenocarcinoma subsets now can be defined by specific 'driver' mutations in genes encoding components of the EGFR signaling pathway. Importantly, these mutations have implications regarding targeted therapy. Here, we focus on EGFR mutant NSCLC-a prime example of a clinically relevant molecular subset of lung cancer, with defined mechanisms of drug sensitivity, primary drug resistance, and acquired resistance to EGFR tyrosine kinase inhibitors. Efforts are now being made to overcome mechanisms of acquired resistance. These findings illustrate how knowledge about the genetic drivers of tumors can lead to rational targeted therapy for individual patients.

MeSH Terms (17)

Animals Antineoplastic Agents Antineoplastic Combined Chemotherapy Protocols Carcinoma, Non-Small-Cell Lung Clinical Trials as Topic Drug Resistance, Neoplasm ErbB Receptors Erlotinib Hydrochloride Gefitinib HSP90 Heat-Shock Proteins Humans Molecular Targeted Therapy Mutation Protein Kinase Inhibitors Protein Structure, Tertiary Quinazolines Quinolines

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