Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC.

[1]  T. Mok,et al.  Gefitinib or carboplatin-paclitaxel in pulmonary adenocarcinoma. , 2009, The New England journal of medicine.

[2]  Y. Yatabe,et al.  Hepatocyte growth factor induces gefitinib resistance of lung adenocarcinoma with epidermal growth factor receptor-activating mutations. , 2008, Cancer research.

[3]  Mehmet Toner,et al.  Detection of mutations in EGFR in circulating lung-cancer cells. , 2008, The New England journal of medicine.

[4]  D. Yee,et al.  Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins. , 2008, The Journal of clinical investigation.

[5]  Alona Muzikansky,et al.  First-line gefitinib in patients with advanced non-small-cell lung cancer harboring somatic EGFR mutations. , 2008, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[6]  P. Jänne,et al.  Preliminary activity and safety results from a phase I clinical trial of PF-00299804, an irreversible pan-HER inhibitor, in patients (pts) with NSCLC , 2008 .

[7]  P. Jänne,et al.  Mechanisms of Acquired Resistance to Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors in Non–Small Cell Lung Cancer , 2008, Clinical Cancer Research.

[8]  S. Kudoh,et al.  Multicentre prospective phase II trial of gefitinib for advanced non-small cell lung cancer with epidermal growth factor receptor mutations: results of the West Japan Thoracic Oncology Group trial (WJTOG0403) , 2008, British Journal of Cancer.

[9]  Li Zhao,et al.  Helical domain and kinase domain mutations in p110α of phosphatidylinositol 3-kinase induce gain of function by different mechanisms , 2008, Proceedings of the National Academy of Sciences.

[10]  M. Meyerson,et al.  The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP , 2008, Proceedings of the National Academy of Sciences.

[11]  M. Meyerson,et al.  PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib. , 2007, Cancer research.

[12]  William Pao,et al.  MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib , 2007, Proceedings of the National Academy of Sciences.

[13]  K. Kiura,et al.  Emergence of epidermal growth factor receptor T790M mutation during chronic exposure to gefitinib in a non small cell lung cancer cell line. , 2007, Cancer research.

[14]  J. Schellens,et al.  First-in-human study of the safety, tolerability, pharmacokinetics (PK), and pharmacodynamics (PD) of PF-00299804, a small molecule irreversible panHER inhibitor in patients with advanced cancer , 2007 .

[15]  Joon-Oh Park,et al.  MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling , 2007, Science.

[16]  Shinji Yamazaki,et al.  An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms. , 2007, Cancer research.

[17]  L. Sequist.  Second-generation epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer. , 2007, The oncologist.

[18]  William Pao,et al.  Novel D761Y and Common Secondary T790M Mutations in Epidermal Growth Factor Receptor–Mutant Lung Adenocarcinomas with Acquired Resistance to Kinase Inhibitors , 2006, Clinical Cancer Research.

[19]  M. Nishimura,et al.  A phase II trial of gefitinib as first-line therapy for advanced non-small cell lung cancer with epidermal growth factor receptor mutations , 2006, British Journal of Cancer.

[20]  P. Jänne,et al.  Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer. , 2006, The Journal of clinical investigation.

[21]  M. Tsuboi,et al.  Analysis of Epidermal Growth Factor Receptor Gene Mutation in Patients with Non–Small Cell Lung Cancer and Acquired Resistance to Gefitinib , 2006, Clinical Cancer Research.

[22]  M. Maemondo,et al.  Prospective phase II study of gefitinib for chemotherapy-naive patients with advanced non-small-cell lung cancer with epidermal growth factor receptor gene mutations. , 2006, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[23]  M. Meyerson,et al.  A Rapid and Sensitive Enzymatic Method for Epidermal Growth Factor Receptor Mutation Screening , 2006, Clinical Cancer Research.

[24]  C. Mermel,et al.  ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[25]  M. Meyerson,et al.  EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. , 2005, The New England journal of medicine.

[26]  H. Varmus,et al.  Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain , 2005, PLoS medicine.

[27]  W. Hofmann,et al.  Presence of the BCR-ABL mutation Glu255Lys prior to STI571 (imatinib) treatment in patients with Ph+ acute lymphoblastic leukemia. , 2003, Blood.

[28]  C. Preudhomme,et al.  A mutation conferring resistance to imatinib at the time of diagnosis of chronic myelogenous leukemia. , 2003, The New England journal of medicine.

[29]  A. D. Van den Abbeele,et al.  Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors. , 2002, The New England journal of medicine.

[30]  J. Kuriyan,et al.  Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid leukemia. , 2002, Cancer cell.

[31]  Claude Preudhomme,et al.  Several types of mutations of the Abl gene can be found in chronic myeloid leukemia patients resistant to STI571, and they can pre-exist to the onset of treatment. , 2002, Blood.

[32]  David I. Smith,et al.  A role for common fragile site induction in amplification of human oncogenes. , 2002, Cancer cell.

[33]  P. N. Rao,et al.  Clinical Resistance to STI-571 Cancer Therapy Caused by BCR-ABL Gene Mutation or Amplification , 2001, Science.

[34]  C. Sawyers,et al.  Activity of a specific inhibitor of the BCR-ABL tyrosine kinase in the blast crisis of chronic myeloid leukemia and acute lymphoblastic leukemia with the Philadelphia chromosome. , 2001, The New England journal of medicine.

[35]  Lin Huan,et al.  Screening for Epidermal Growth Factor Receptor Mutations in Lung Cancer , 2010 .