Mechanisms of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non–Small Cell Lung Cancer

By J. Engelman, P. Jänne. Clinical Cancer Research, 2008

696 citations recorded by the source corpus.

Subfields: Oncology, Pulmonary and Respiratory Medicine, Surgery

View Paper: https://www.semanticscholar.org/paper/48d1fc3f8ad2d16897592042668214e499a07eba

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. J. Engelman
2. Gwen Macdonald
3. N. Hynes
4. P. Jänne
5. D. Hanahan
6. R. Weinberg

In Pulmonary and Respiratory Medicine

1. J. Engelman
2. L. Sequist
3. N. Hynes
4. Gwen Macdonald
5. P. Jänne
6. R. Weinberg
7. D. Hanahan

In Surgery

1. J. Engelman

Citations in the corpus

• Pre-existence and clonal selection of MET amplification in EGFR mutant NSCLC (2010, background): “Both resistance mechanisms lead to maintenance of ERBB3/PI3K/AKT signaling in the presence of gefitinib (reviewed in Engelman and Janne, 2008 ).”
• 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): “Alternate pathways of TKI resistance, of which several have been hypothesized (39), are actively being investigated by multiple groups using high throughput mutation testing, siRNA screens, and gene expression microarray analysis.”
• ErbB receptors and signaling pathways in cancer. (2009, background): “The same holds true for NSCLC patients whose tumors have a mutant EGFR, since even if there is a strong initial clinical response to gefitinib or erlotinib, the response only lasts 6–12 months [15].”