ZD1839 (Iressa): an orally active inhibitor of epidermal growth factor signaling with potential for cancer therapy.
By A. Wakeling, S. P. Guy, J. Woodburn, S. Ashton, B. Curry, A. Barker, K. Gibson. Cancer Research, 2002
956 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/69be710b05b2980b807b59aaa16fecc4e4dcfbac
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Citations in the corpus
- A Unique Structure for Epidermal Growth Factor Receptor Bound to GW572016 (Lapatinib) (2004, methodology): “Exposure to kinase inhibitors causes the down-regulation of tyrosine phosphorylation of ErbB receptors in tumor cells ( 4 , 5, 7). We examined the recovery of receptor phosphorylation after inhibitor washout to determine whether there is a correlation between inhibitor dissociation rate and recovery”
- Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer. (2004, background): “33 mol/L, which is 100 times lower than the concentration required to block the kinases of HER-2, KDR, MEK-1, and MEK-2 [2].”
- Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial. (2003, unknown): “Radiographic response rate [95% CI] 12 (12) [6-20] 10 (9) [4-16] 22 (10) [6-14] .”
- Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity. (2007, background): “…of these inhibitors are currently in clinical trials or have been approved for clinical use, including the 4-anilinoquinazolines gefitinib (Iressa) (Wakeling et al., 2002), erlotinib (Tarceva) (Pollack et al., 1999), and lapatinib (Rusnak et al., 2001); the pyrrolopyrimidine AEE788 (Traxler et…”
- Antitumor Activity of HKI-272, an Orally Active, Irreversible Inhibitor of the HER-2 Tyrosine Kinase (2004, background): “Although this compound is much less active against HER-2 in cell-free systems (38), it has been reported to inhibit the growth of HER-2-expressing cells in vitro and in vivo (24, 39).”