EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib.
By William Pao, Vincent A. Miller, M. Zakowski, J. Doherty, K. Politi, I. Sarkaria, Bhuvanesh Singh, R. Heelan, V. Rusch, L. Fulton and 5 more. Proceedings of the National Academy of Sciences of the United States of America, 2004
3,941 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/24811c3347c1a54faea85a73e0c6b38d00c8e2e7
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In Oncology
- William Pao
- P. Jänne
- Gregory Riely
- Adi F. Gazdar
- Vincent A. Miller
- M. Kris
- C. Zappa
- Christopher Sander
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity. (2007, background): “In particular, the L858R mutant is 10- to 100-fold more sensitive to erlotinib and gefitinib than the wild-type kinase (Pao et al., 2004; Greulich et al., 2005; Mukohara et al., 2005) and significantly more sensitive than the G719S mutant (Jiang et al., 2005).”