Analysis of Epidermal Growth Factor Receptor Gene Mutation in Patients with Non–Small Cell Lung Cancer and Acquired Resistance to Gefitinib
By T. Kosaka, Yasushi Yatabe, H. Endoh, Kimihide Yoshida, T. Hida, M. Tsuboi, H. Tada, H. Kuwano, T. Mitsudomi. Clinical Cancer Research, 2006
605 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/d3df93f7355e72ffeabe0dd5984683f341334c8d
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Oncology
In Pulmonary and Respiratory Medicine
Citations in the corpus
- The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP (2008, background): “The T790M mutation accounts for about half of all resistance to gefitinib and erlotinib (16, 17).”
- Pre-existence and clonal selection of MET amplification in EGFR mutant NSCLC (2010, background): “Secondary mutations in EGFR itself, including the EGFR T790M ‘‘gatekeeper’’ mutation is observed in 50% of resistance cases, and amplification of the MET oncogene is observed in 20% of resistance cases (Balak et al., 2006; Bean et al., 2007; Engelman et al., 2007b; Kobayashi et al., 2005; Kosaka et ”
- Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors (2009, neutral): “The threonine-790 to methionine (T790M) point mutation is found in approximately 50% of all patients at the time of acquired resistance to EGFR TKI therapy (Kobayashi et al., 2005; Balak et al., 2006; Kosaka et al., 2006).”