Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer.

By Vincent A. Miller, M. Kris, N. Shah, J. Patel, C. Azzoli, Jorge E Gomez, L. Krug, William Pao, N. Rizvi, B. Pizzo and 7 more. Journal of Clinical Oncology, 2004

753 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/db26aaed91573d90fd091d6a3cdefdca1e90ecbc

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. B. Riggs
3. C. Sawyers
4. J. Chmielecki
5. E. Scholar
6. A. Arora

In Pulmonary and Respiratory Medicine

1. B. Hughes
2. B. Chan
3. J. Chmielecki
4. William Pao
5. C. Sawyers

Citations in the corpus

• Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors. (2005, background): “Coexpression of EGFRvIII and PTEN‡ 6/7 (86) 2/19 (11) <0.”
• Molecular Testing Guideline for Selection of Lung Cancer Patients for EGFR and ALK Tyrosine Kinase Inhibitors (2013, neutral): “As gefitinib and erlotinib, small-molecule competitive inhibitors of the EGFR tyrosine kinase, were being evaluated in clinical trials of advanced-stage lung cancer in the early part of the last decade, unusual prolonged responses to these medications were recognized in a subset of patients.(2) This”
• Erlotinib in lung cancer - molecular and clinical predictors of outcome. (2005, neutral): “<60 yr 149 (46) 49 (39) 79 (45) 332 (45) ≥60 yr 176 (54) 76 (61) 98 (55) 399 (55) Sex Female 115 (35) 44 (35) 66 (37) 256 (35) Male 210 (65) 81 (65) 111 (63) 475 (65) Performance status 0 or 1 203 (62) 91 (73) 127 (72) 486 (66) 2 or 3 122 (38) 34 (27) 50 (28) 245 (34) P value 0.”
• Hepatocyte growth factor induces gefitinib resistance of lung adenocarcinoma with epidermal growth factor receptor-activating mutations. (2008, background): “It is well known that nonsmokers with lung cancer show a more favorable response to gefitinib than smokers (34).”
• Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors (2009, neutral): “Thus, the frequency of the EGFR mutation mirrors the clinically defined subgroups of patients who were most likely to achieve radiographic responses to EGFR TKIs (Miller and Kris, 2004).”
• Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer (2010, background): “( Table 1 ), the major clinical characteristics of responding patients were found to be adenocarcinoma histology, East Asian ethnicity, a history of never smoking cigarettes and female gende”