Screening for Epidermal Growth Factor Receptor Mutations in Lung Cancer

By Lin Huan. 2010

1,444 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/eb4255d0df483cdb99729f92c05343314d4ef95a

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Citations in the corpus

Targeted therapy for non-small cell lung cancer: current standards and the promise of the future. (2015, background): “org resulting in constitutive activation of the receptor without ligand binding (21-23).”
Identification of genes upregulated in ALK-positive and EGFR/KRAS/ALK-negative lung adenocarcinomas. (2012, background): “EGFR mutations make tumor cells dependent on epidermal growth factor receptor (EGFR) signaling and define patients who respond to EGFR tyrosine kinase inhibitors (TKI), such as gefitinib (10, 11).”
An ultrasensitive method for quantitating circulating tumor DNA with broad patient coverage (2014, unknown): “P6 54 M Adeno IV T3N2M1b None 3 (2) 0 ALK KIF5B 1.”
First-line erlotinib versus gemcitabine/cisplatin in patients with advanced EGFR mutation-positive non-small-cell lung cancer: analyses from the phase III, randomized, open-label, ENSURE study. (2015, background): “EGFR mutations occur more frequently in Asian patients compared with Caucasian patients (30% and ∼16%, respectively) [3–5].”
Pre-existence and clonal selection of MET amplification in EGFR mutant NSCLC (2010, background): “This approach is clinically appealing because combined treatment with an EGFR and MET inhibitor, specifically in patients with evidence of MET amplification at baseline, may lead to a longer time to progression than is currently observed with gefitinib or erlotinib alone (Asahina et al., 2006; Inoue”
Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer (2010, background): “Erlotinib has similarly been shown to be highly effective in patients with EGFR -mutant tumour”