Determinants of tumor response and survival with erlotinib in patients with non--small-cell lung cancer.
By R. Perez-soler, A. Chachoua, L. Hammond, E. Rowinsky, M. Huberman, D. Karp, J. Rigas, G. Clark, P. Santabarbara, P. Bonomi. Journal of Clinical Oncology, 2004
1,103 citations recorded by the source corpus.
Subfields: Oncology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/f195651181beab1afa2018a65f99a1b7f85d7fae
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In Oncology
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Comparing antibody and small-molecule therapies for cancer (2006, background): “In a series of clinical trials, gefitinib and erlotinib caused objective responses in 10–20% of previously treated patients with NSCL”
- Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors (2009, neutral): “Treatment with the reversible EGFR TK inhibitors (TKIs), gefitinib and erlotinib, results in dramatic antitumor activity in a subset of patients with NSCLC: clinical responses have been achieved in approximately 10% of European patients and in 30% of patients from East Asia (Fukuoka et al., 2003; Kr”
- Targeted therapy for non-small cell lung cancer: current standards and the promise of the future. (2015, methodology): “Early trials used EGFR TKIs in an unselected population as these predated the now known clinical and molecular predictive biomarkers (24-28).”
- Clinical signs, pathophysiology and management of skin toxicity during therapy with epidermal growth factor receptor inhibitors. (2005, background): “First, similar cutaneous effects develop regardless of the mechanism of action of the EGFR inhibitor as a monoclonal antibody (cetuximab, panitumumab, matuzumab) [2‐5, 17] or as an EGFR-specific tyrosine kinase inhibitor (gefitinib, erlotinib) [12, 14, 15, 18 ].”
- Erlotinib in lung cancer - molecular and clinical predictors of outcome. (2005, background): “Low trisomy (3 gene copies in 10–39% of cells) 23 (18)”