Erlotinib in previously treated non-small-cell lung cancer.

By F. Shepherd, J. Rodrigues Pereira, T. Ciuleanu, E. Tan, V. Hirsh, S. Thongprasert, D. Campos, Savitree Maoleekoonpiroj, M. Smylie, R. Martins and 9 more. New England Journal of Medicine, 2005

4,948 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/0b6f3a3a1759d7b979deeab63547aaecb54edf42

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The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Oncology

1. Andrew K. Joe
2. F. Hodi
3. D. Pardoll
4. S. Topalian
5. William Pao
6. K. Borden
7. H. Zahreddine
8. I. Weinstein

In Pulmonary and Respiratory Medicine

1. Michael R. Kosorok
2. B. Hughes
3. B. Chan
4. Adi F. Gazdar
5. S. Lippman
6. L. Sequist
7. William Pao
8. Eric B. Laber

Citations in the corpus

• KRAS Mutation Is an Important Predictor of Resistance to Therapy with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non–Small-Cell Lung Cancer (2007, neutral): “Positive Positive Negative 5 4 (80) 0 1 (20) Negative Positive Negative 19 0 5 (26) 14 (74) Negative Negative Negative 20 1 (5) 3 (15) 16 (80) Positive Negative Negative 1 0 0 1 (100) Negative Positive Positive 8 0 0 8 (100) Negative Negative Positive 6 0 0 6 (100) Table 4.”
• 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”
• Reinforcement learning design for cancer clinical trials (2009, neutral): “In our future study we will apply reinforcement learning to discover individualized optimal regimens while restricting attention to first-line and second-line only, since there is only one approved agent (Erlotinib) indicated for third-line treatment [38].”
• Targeting the EGFR signaling pathway in cancer therapy (2012, background): “A randomized study in patients having advanced NSCLC and who had failed standard cytotoxic chemotherapy showed improved clinical symptoms and a better survival rate with erlotinib [84,86,87].”
• EGFR and EphA2 are host factors for hepatitis C virus entry and possible targets for antiviral therapy (2011, neutral): “2341-S1">Supplementary Table 2 ) and their kinase function is inhibited by clinically approved protein kinase inhibitors (PKIs”
• The BATTLE Trial: Personalizing Therapy for Lung Cancer (2011, result): “Our overall response rate of 4% is reflective of a heavily pretreated NSCLC population and consistent with other published studies in this population (5, 9, 14).”
• 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): “Erlotinib has proven efficacy as second-/third-line treatment of advanced NSCLC [7], and superior first-line efficacy versus chemotherapy in EGFR mutation-positive disease [8–11].”
• Reinforcement Learning Strategies for Clinical Trials in Non-small Cell Lung Cancer (2011, background): “Food and Drug Administration (FDA)-approved secondline agents (docetaxel, pemetrexed, and erlotinib) appear to have similar response and overall survival efficacy but very different toxicity profiles (Shepherd et al., 2005; Ciuleanu et al., 2009).”
• Lung cancer in never smokers — a different disease (2007, background): “These observations led to the development and widespread clinical testing of small-molecule tyrosine kinase inhibitors (TKIs) including erlotinib (Tarceva) and gefitinib (Iressa”
• Phase III study of afatinib or cisplatin plus pemetrexed in patients with metastatic lung adenocarcinoma with EGFR mutations. (2013, background): “Gefitinib and erlotinib were initially considered salvage therapies, with low response rates but marginal improvement in survival compared with placebo in unselected patients.(19,20) Once the qualitative difference in response to EGFR TKIs among EGFR-mutant patients was appreciated, randomized studi”