Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR.

By M. Maemondo, A. Inoue, K. Kobayashi, S. Sugawara, S. Oizumi, H. Isobe, A. Gemma, M. Harada, H. Yoshizawa, I. Kinoshita and 13 more. New England Journal of Medicine, 2010

864 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/76fb538feeb76533fc03bed67f17018724500ca8

How researchers see this paper

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

In Oncology

1. William Pao
2. Gregory Riely
3. Vincent A. Miller
4. M. Kris

In Pulmonary and Respiratory Medicine

1. William Pao
2. Gregory Riely
3. Vincent A. Miller
4. M. Kris
5. Marc Ladanyi
6. Jin-Yuan Shih
7. Shang-Gin Wu

Citations in the corpus

• Predicting EGFR mutation status in lung adenocarcinoma on computed tomography image using deep learning (2019, background): “Lung adenocarcinoma is a common histological type of lung cancer and the discovery of epidermal growth factor receptor (EGFR) mutations has revolutionised its treatment [1, 2].”
• Acquired resistance to EGFR tyrosine kinase inhibitors in EGFR mutant lung cancer: Distinct natural history of patients with tumors harboring the T790M mutation (2010, neutral): “Median time from progression to new metastatic organ involvement, months* 14 (8-18) 4 (1-9) 0.”
• Systemic Therapy for Stage IV Non-Small-Cell Lung Cancer: American Society of Clinical Oncology Clinical Practice Guideline Update. (2016, background): “There were 51 trials in the first-line and maintenance settings, including seven trials for the treatment of patients with epidermal growth factor receptor (EGFR) mutations or increased EGFR expression.(11,13,14,20,29-32) Twenty-five trials included patients with multiple histologies (including squa”
• HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation. (2012, background): “Tumors with the most common alterations, exon 19 deletions and exon 21 point mutations (L858R), are initially responsive to EGFR tyrosine kinase inhibitors (TKIs) such as gefitinib or erlotinib (4, 5) but eventually acquire resistance.”