Responsiveness to EGFR tyosine kinase inhibitors in lung cancer
Non-small cell lung cancer (NSCLC) is one of the most common cancers worldwide. Pulmonary malignancies are the leading cause of death in both men and women1. Treatment generally consists of surgical resection, radiation therapy and/or chemotherapy. Somatic mutations within the kinase domain (exons 18-21) of the epidermal growth factor receptor (EGFR) gene have been reported for 10-35% of NSCLC tumors2, 4, 5. Multiple studies have demonstrated a strong association of EGFR mutation status with response to EGFR tyrosine kinase inhibitors, gefitinib and erlotinib3, 4, 5.
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(Targeted analysis for 123 cancer hotspot mutations in the EGFR gene by next generation sequencing.)
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- Ries LAG, Kosary CL, Hankey BF, et al, editors. “SEER Cancer Statistics Review, 1973 1996”. Bethesda, MD: National Cancer Institute; 1999.
- Lynch et al., Activiating Mutations in the Epidermal Growth Factor Receptor Underlying Responsiveness of Non-Small-Cell Lung Cancer to Gefitinib. NEJM, 2004; 350(21): 2129-2139.
- Fukuoka, M., Yano, S., Giaccone, G., et al., “Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer., J. Clin. Oncol.;21:2237-46, 2003.
- Paez et al., EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy. Science, 2004; 304: 1497-1500.
- Pao et al., EGF receptor gene mutations are common in lung cancers from “never smokers” and are associated with sensitivity of tumors to gefitinib and erlotinib. PNAS, 2004; 101(36): 13306-13311.
- Pao et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med. 2005 Mar;2(3):e73.