Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib.

By Thomas J. Lynch, D. Bell, Raffaella Sordella, S. Gurubhagavatula, Ross A. Okimoto, Brian W. Brannigan, Patricia L. Harris, Sara M. Haserlat, J. Supko, F. Haluska and 4 more. New England Journal of Medicine, 2004

1,608 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/0454ec510925e554634231d478e1f00a7ea3c787

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In Oncology

In Pulmonary and Respiratory Medicine

Citations in the corpus

Molecular Testing Guideline for Selection of Lung Cancer Patients for EGFR and ALK Tyrosine Kinase Inhibitors (2013, neutral): “Although this method, with this level of performance, was the initial method used to establish the value of the test for predicting response of tumors to erlotinib and gefitinib, many specimens fall short of this tumor content.(47,161,162) As a consequence, laboratories exclusively using this method”
MET Exon 14 Mutations in Non-Small-Cell Lung Cancer Are Associated With Advanced Age and Stage-Dependent MET Genomic Amplification and c-Met Overexpression. (2016, neutral): “10 15 (53) 28 (28) 152 (90) Race White, non-Hispanic 28 (100) 79 (80) 157 (93) Asian 0 (0) 15 (15) 0 (0) Black 0 (0) 1 (1) 5 (3) White, Hispanic 0 (0) 3 (3) 3 (2) Unknown 0 (0) 1 (1) 4 (2) Histology Adenocarcinoma 18 (64) 92 (93) 150 (89) Pleomorphic with adenocarcinoma component 4 (14) 0 (0) 3 (2) ”
Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. (2007, positive): “…(Table 2); of these, 9/16 tumors show kinase domain-activating mutations with 8/8 adenocarcinomas and 5/5 female nonsmokers showing EGFR-activating mutations, consistent with previous reports of enrichment for female nonsmokers and adenocarcinoma (Lynch et al., 2004; Pao et al., 2004) (Table 2).”
Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity. (2007, background): “…EGFR mutant tumors and cell lines may derive from an ‘‘oncogene addiction’’ effect (Gazdar et al., 2004), it may also stem, at least in part, from structural differences in the mutant kinases that confer intrinsic susceptibility to particular inhibitors (Lynch et al., 2004; Greulich et al., 2005).”
AZD9291 in EGFR inhibitor-resistant non-small-cell lung cancer. (2015, neutral): “Grade 3–5 0 1 (2) 1 (1) 1 (2) 1 (5) 4 (2)”
Unique Clinicopathologic Features Characterize ALK-rearranged Lung Adenocarcinoma in the Western Population (2009, result): “The characteristics of NSCLC with ALK rearrangements in our study are very similar to those for NSCLC harboring mutations in EGFR (30, 31).”
Sunitinib in patients with metastatic renal cell carcinoma. (2006, neutral): “Lung 51 (81) 86 (82) 137 (82) Liver 10 (16) 28 (27) 38 ( 23 )”
Target Binding Properties and Cellular Activity of Afatinib (BIBW 2992), an Irreversible ErbB Family Blocker (2012, background): “, L858R point mutation or exon 19 deletions) have been identified and validated as cancer-promoting mechanisms (Lynch et al., 2004; Ji et al., 2006).”
Overcoming EGFR T790M and C797S resistance with mutant-selective allosteric inhibitors (2016, neutral): “The L858R point mutation and small, in-frame deletions in the region encoded by exon 19 are the most common mutations, and are among a subset of oncogenic EGFR alterations that confer enhanced sensitivity to EGFR-directed TKIs 11-13 .”
Circulating tumor cells: approaches to isolation and characterization (2011, neutral): “In nonsmokers’ lung cancer, EGF receptor (EGFR) mutations are particularly relevant because they are predictive of a dramatic clinical response to EGFR kinase inhibitors (Lynch et al., 2004; Paez et al., 2004; Pao et al., 2004).”