First-line gefitinib in patients with advanced non-small-cell lung cancer harboring somatic EGFR mutations.

By L. Sequist, R. Martins, D. Spigel, S. Grunberg, A. Spira, P. Jänne, V. Joshi, D. McCollum, T. Evans, A. Muzikansky and 9 more. Journal of Clinical Oncology, 2008

865 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/29a226970227068f01ac54d350b0e282eee8e147

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In Oncology

In Pulmonary and Respiratory Medicine

Citations in the corpus

AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer (2014, neutral): “Studies using more conventional diagnostic assays have reported detection in about 2% of TKI-naïve tumors (56).”
Pre-existence and clonal selection of MET amplification in EGFR mutant NSCLC (2010, background): “Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib are effective clinical therapies for patients with advanced non-small cell lung cancer (NSCLC) who have EGFR-activating mutations (Asahina et al., 2006; Inoue et al., 2006; Rosell et al., 2009; Sequist ”
Nanomedicine therapeutic approaches to overcome cancer drug resistance (2013, background): “Somatic mutations resulting in a gain-of-function activation of the tyrosine kinase domain of EGFR in a cohort of non-small cell lung cancer (NSCLC) were discovered in 35% of the enrolled patients and were shown to significantly impact response rates to gefitinib (55%) [51].”
A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors (2011, background): “Acquired drug resistance mechanisms can sometimes also occur de novo and both EGFR T790M and MET amplification have been described in cancers from EGFR TKI naive patients(26).”