Year: 2011
Type: editorial
Abstract: Interest in activating “driver” mutations in tyrosine kinase genes as therapeutic targets in non-small cell lung cancer (NSCLC) has peaked recently due to the discovery that EGFR tyrosine kinase inhibitors (TKIs) produce higher response rates, longer progression free survival (PFS) times, less toxicity, improved symptom control, improved quality of life, and greater convenience compared to cytotoxic chemotherapy in the first line treatment of advanced NSCLC patients harboring EGFR activating mutations (1–4). A more recent study showed that advanced NSCLC patients whose tumors harbor EML4-ALK fusion genes, who are treated with an ALK TKI termed crizotinib, have high response rates and long progression free survival times that are similar to those of NSCLC patients harboring EGFR mutations treated with erlotinib (5,6).
Source: Journal of Clinical Oncology
Authors: Paul A. Bunn, Robert C. Doebele
Institution: University of Colorado Cancer Center
Language: English
Subfield: Genetics
Domain: Life Sciences
Open Access status: bronze
OpenAlex ID: W2120201414