Clinical Course of Patients with Non–Small Cell Lung Cancer and Epidermal Growth Factor Receptor Exon 19 and Exon 21 Mutations Treated with Gefitinib or Erlotinib
By Gregory Riely, William Pao, Duykhanh Pham, Allan R. Li, N. Rizvi, E. Venkatraman, M. Zakowski, M. Kris, Marc Ladanyi, Vincent A. Miller. Clinical Cancer Research, 2006
736 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/38742ec1586a1a06c37c25cc8516ccb92449ef63
How researchers see this paper
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In Oncology
- William Pao
- J. Engelman
- P. Jänne
- Gregory Riely
- Vincent A. Miller
- M. Kris
- G. Shapiro
- James E. Bradner
In Pulmonary and Respiratory Medicine
- William Pao
- J. Engelman
- Gregory Riely
- P. Jänne
- Vincent A. Miller
- M. Kris
- Marc Ladanyi
- James E. Bradner
Citations in the corpus
- PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib. (2007, background): “In patients treated with gefitinib or erlotinib, the median time to progression and overall survival is significantly longer for patients whose tumors contain exon 19 deletions compared with those with L858R (50, 51).”
- Clinical characteristics of patients with lung adenocarcinomas harboring BRAF mutations. (2011, background): “It will be interesting to see whether a comparable difference in clinical behavior is seen among these mutations, either within or outside the context of a specific treatment, as has been demonstrated with the two predominant EGFR mutation subtypes after treatment with erlotinib (exon 19 deletion, e”
- Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors (2009, neutral): “Response rates to EGFR TKIs are higher in patients with NSCLC, whose tumors have exon 19 mutations (70–100%), than in patients with exon 21 mutations (20–67%) (Mitsudomi et al., 2005; Hirsch et al., 2006; Jackman et al., 2006; Riely et al., 2006).”
- Novel D761Y and Common Secondary T790M Mutations in Epidermal Growth Factor Receptor–Mutant Lung Adenocarcinomas with Acquired Resistance to Kinase Inhibitors (2006, background): “whose tumors harbor EGFR exon 19 deletion mutations have a longer median survival than those with EGFR L858R point mutation (5).”