Gefitinib-Sensitizing EGFR Mutations in Lung Cancer Activate Anti-Apoptotic Pathways
By Raffaella Sordella, D. Bell, D. Haber, J. Settleman. Science, 2004
1,654 citations recorded by the source corpus.
Subfields: Oncology, Pathology and Forensic Medicine, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/80b47e819057cb298e40fa1b2a39f1723517bd3d
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In Oncology
- William Pao
- P. Jänne
- Adi F. Gazdar
- Andrew K. Joe
- Gregory Riely
- Vincent A. Miller
- H. Shigematsu
- Gwen Macdonald
In Pathology and Forensic Medicine
In Pulmonary and Respiratory Medicine
Citations in the corpus
- The modulation of ABC transporter-mediated multidrug resistance in cancer: a review of the past decade. (2015, background): “Gefitinib Gefitinib, an inhibitor of EGFR (ErbB1), has been approved for he treatment of non-small cell lung cancer (Pao et al., 2004; ordella et al., 2004).”
- Mechanisms of Disease: oncogene addiction—a rationale for molecular targeting in cancer therapy (2006, background): “An experimental study indicated that mutations in the EGFR can preferentially enhance activation of the survival, Akt-associated pathway”
- Input–output behavior of ErbB signaling pathways as revealed by a mass action model trained against dynamic data (2009, background): “H1666 and H3255 cell lines, which carry wild-type and mutant L858R ErbB1 receptors (Sordella et al , 2004; Tracy, 2004), respectively, were studied to ascertain whether the IERMv1.”
- Targeted cancer therapy (2004, methodology): “A third example is to use inhibitors of kinases in the PI(3)K/Akt/mTOR pathway to treat tumours with mutations in the tumour suppressor gene PTEN — the negative principal regulator of this pathway (see reviews in this issue by Massagué, page 298, and by Lowe et al.”
- ErbB receptors and signaling pathways in cancer. (2009, background): “Considering lung cancer, the prosurvival PI3K/Akt and STAT pathways appear to be hyperactive in the context of mutant EGFRs [25,26].”
- Oncogenic Transformation by Inhibitor-Sensitive and -Resistant EGFR Mutants (2005, background): “Ligand-independent activation of EGFR with lung cancer-derived kinase domain mutations has not been observed by other groups working with transient transfection systems [22,27].”