Mutations in the tyrosine kinase domain of the EGFR gene associated with gefitinib response in non-small-cell lung cancer.

[1]  S. Steinberg,et al.  ras gene mutations in non-small cell lung cancers are associated with shortened survival irrespective of treatment intent. , 1991, Cancer research.

[2]  L. V. van't Veer,et al.  Mutational activation of the K-ras oncogene and the effect of chemotherapy in advanced adenocarcinoma of the lung: a prospective study. , 1997, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[3]  Joe W. Gray,et al.  PIK3CA is implicated as an oncogene in ovarian cancer , 1999, Nature Genetics.

[4]  W. Alvord,et al.  Ras Oncogene-Induced Sensitization to 1-β-d-Arabinofuranosylcytosine , 1999 .

[5]  M. van Glabbeke,et al.  New guidelines to evaluate the response to treatment in solid tumors , 2000, Journal of the National Cancer Institute.

[6]  M. Spitz,et al.  Repair of tobacco carcinogen-induced DNA adducts and lung cancer risk: a molecular epidemiologic study. , 2000, Journal of the National Cancer Institute.

[7]  R. Simon,et al.  Length and loss of heterozygosity of an intron 1 polymorphic sequence of egfr is related to cytogenetic alterations and epithelial growth factor receptor expression. , 2000, Cancer research.

[8]  T. Hunter,et al.  Oncogenic kinase signalling , 2001, Nature.

[9]  A. Nicholson,et al.  Mutations of the BRAF gene in human cancer , 2002, Nature.

[10]  M. Sliwkowski,et al.  Structure of the Epidermal Growth Factor Receptor Kinase Domain Alone and in Complex with a 4-Anilinoquinazoline Inhibitor* , 2002, The Journal of Biological Chemistry.

[11]  G. Mills,et al.  Loss of PTEN/MMAC1/TEP in EGF receptor-expressing tumor cells counteracts the antitumor action of EGFR tyrosine kinase inhibitors , 2003, Oncogene.

[12]  Masahiro Fukuoka,et al.  Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer (The IDEAL 1 Trial) [corrected]. , 2003, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[13]  David Cella,et al.  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, JAMA.

[14]  Patricia L. Harris,et al.  Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. , 2004, The New England journal of medicine.

[15]  J. Ptak,et al.  High Frequency of Mutations of the PIK3CA Gene in Human Cancers , 2004, Science.

[16]  S. Gabriel,et al.  EGFR Mutations in Lung Cancer: Correlation with Clinical Response to Gefitinib Therapy , 2004, Science.

[17]  R. Wilson,et al.  EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[18]  Roy S Herbst,et al.  Gefitinib in combination with paclitaxel and carboplatin in advanced non-small-cell lung cancer: a phase III trial--INTACT 2. , 2004, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[19]  G. Giaccone,et al.  Gefitinib in combination with gemcitabine and cisplatin in advanced non-small-cell lung cancer: a phase III trial--INTACT 1. , 2004, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[20]  Daniel A. Haber,et al.  Gefitinib-Sensitizing EGFR Mutations in Lung Cancer Activate Anti-Apoptotic Pathways , 2004, Science.

[21]  M. Kuwano,et al.  Sensitivity to gefitinib (Iressa, ZD1839) in non-small cell lung cancer cell lines correlates with dependence on the epidermal growth factor (EGF) receptor/extracellular signal-regulated kinase 1/2 and EGF receptor/Akt pathway for proliferation. , 2004, Molecular cancer therapeutics.

[22]  T. Crook,et al.  Polymorphism in wild-type p53 modulates response to chemotherapy in vitro and in vivo , 2004, Oncogene.

[23]  J. Dancey.  Predictive factors for epidermal growth factor receptor inhibitors--the bull's-eye hits the arrow. , 2004, Cancer cell.

[24]  C. Harris,et al.  Tobacco Carcinogen-Induced Cellular Transformation Increases Activation of the Phosphatidylinositol 3′-Kinase/Akt Pathway in Vitro and in Vivo , 2004, Cancer Research.

[25]  William Pao,et al.  Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer. , 2004, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.