Vandetanib is effective in EGFR-mutant lung cancer cells with PTEN deficiency.

[1]  Yuki Togashi,et al.  RET, ROS1 and ALK fusions in lung cancer , 2012, Nature Medicine.

[2]  A. Tsao.  Vandetanib Versus Placebo in Patients With Advanced Non–Small-Cell Lung Cancer After Prior Therapy With an Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor: A Randomized, Double-Blind Phase III Trial (ZEPHYR) , 2012 .

[3]  Edward S. Kim,et al.  The BATTLE trial: personalizing therapy for lung cancer. , 2011, Cancer discovery.

[4]  H. Hieronymus,et al.  FAS and NF-κB signalling modulate dependence of lung cancers on mutant EGFR , 2011, Nature.

[5]  S. Digumarthy,et al.  Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors , 2011, Science Translational Medicine.

[6]  Chih-Hsin Yang,et al.  Vandetanib plus pemetrexed for the second-line treatment of advanced non-small-cell lung cancer: a randomized, double-blind phase III trial. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[7]  Michael Thomas,et al.  Phase III trial of vandetanib compared with erlotinib in patients with previously treated advanced non-small-cell lung cancer. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[8]  H. Uramoto,et al.  Cancer esearch apeutics , Targets , and Chemical Biology s of PTEN Expression by Blocking Nuclear Translocation GR 1 in Gefitinib-Resistant Lung Cancer Cells Harboring R ermal Growth Factor Receptor – Activating Mutations , 2010 .

[9]  Dong Sun Kim,et al.  PTEN mutations and relationship to EGFR, ERBB2, KRAS, and TP53 mutations in non-small cell lung cancers. , 2010, Lung cancer.

[10]  Yan Sun,et al.  Vandetanib plus docetaxel versus docetaxel as second-line treatment for patients with advanced non-small-cell lung cancer (ZODIAC): a double-blind, randomised, phase 3 trial. , 2010, The Lancet. Oncology.

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

[12]  K. Kiura,et al.  Effects of vandetanib on lung adenocarcinoma cells harboring epidermal growth factor receptor T790M mutation in vivo. , 2009, Cancer research.

[13]  R. Herbst,et al.  Baseline Vascular Endothelial Growth Factor Concentration as a Potential Predictive Marker of Benefit from Vandetanib in Non–Small Cell Lung Cancer , 2009, Clinical Cancer Research.

[14]  P. Jänne,et al.  Combined Vascular Endothelial Growth Factor Receptor and Epidermal Growth Factor Receptor (EGFR) Blockade Inhibits Tumor Growth in Xenograft Models of EGFR Inhibitor Resistance , 2009, Clinical Cancer Research.

[15]  M. Meyerson,et al.  PTEN loss contributes to erlotinib resistance in EGFR-mutant lung cancer by activation of Akt and EGFR. , 2009, Cancer research.

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

[17]  Pier Paolo Pandolfi,et al.  Tenets of PTEN Tumor Suppression , 2008, Cell.

[18]  Y. Yatabe,et al.  Mutations of the epidermal growth factor receptor gene and related genes as determinants of epidermal growth factor receptor tyrosine kinase inhibitors sensitivity in lung cancer , 2007, Cancer science.

[19]  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.

[20]  M. Kris,et al.  Phase 1 trial of everolimus and gefitinib in patients with advanced nonsmall‐cell lung cancer , 2007, Cancer.

[21]  G. Mills,et al.  Acquired resistance to erlotinib in A-431 epidermoid cancer cells requires down-regulation of MMAC1/PTEN and up-regulation of phosphorylated Akt. , 2007, Cancer research.

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

[23]  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.

[24]  G. Giaccone,et al.  Enhanced cytotoxicity induced by gefitinib and specific inhibitors of the Ras or phosphatidyl inositol-3 kinase pathways in non-small cell lung cancer cells. , 2006, International journal of cancer.

[25]  N. Hanna,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 , 2006 .

[26]  Koji Yoshimoto,et al.  Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors. , 2005, The New England journal of medicine.

[27]  E. Brown,et al.  Epithelial to mesenchymal transition is a determinant of sensitivity of non-small-cell lung carcinoma cell lines and xenografts to epidermal growth factor receptor inhibition. , 2005, Cancer research.

[28]  H. Hurwitz,et al.  Clinical evaluation of ZD6474, an orally active inhibitor of VEGF and EGF receptor signaling, in patients with solid, malignant tumors. , 2005, Annals of oncology : official journal of the European Society for Medical Oncology.

[29]  A. Ryan,et al.  ZD6474 – a novel inhibitor of VEGFR and EGFR tyrosine kinase activity , 2005, British Journal of Cancer.

[30]  A. Yoshimura,et al.  Reduction of PTEN protein and loss of epidermal growth factor receptor gene mutation in lung cancer with natural resistance to gefitinib (IRESSA) , 2005, British Journal of Cancer.

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

[32]  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.

[33]  Joachim Herz,et al.  Mutations and addiction to EGFR: the Achilles 'heal' of lung cancers? , 2004, Trends in molecular medicine.

[34]  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.

[35]  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.

[36]  D. Chung,et al.  Down-regulation of the Tumor Suppressor PTEN by the Tumor Necrosis Factor-α/Nuclear Factor-κB (NF-κB)-inducing Kinase/NF-κB Pathway Is Linked to a Default IκB-α Autoregulatory Loop* , 2004, Journal of Biological Chemistry.

[37]  D. Chung,et al.  Down-regulation of the tumor suppressor PTEN by the tumor necrosis factor-alpha/nuclear factor-kappaB (NF-kappaB)-inducing kinase/NF-kappaB pathway is linked to a default IkappaB-alpha autoregulatory loop. , 2004, The Journal of biological chemistry.

[38]  Q. She,et al.  Resistance to gefitinib in PTEN-null HER-overexpressing tumor cells can be overcome through restoration of PTEN function or pharmacologic modulation of constitutive phosphatidylinositol 3'-kinase/Akt pathway signaling. , 2003, Clinical cancer research : an official journal of the American Association for Cancer Research.

[39]  B. Curry,et al.  ZD6474 inhibits vascular endothelial growth factor signaling, angiogenesis, and tumor growth following oral administration. , 2002, Cancer research.

[40]  Li Mao,et al.  Lack of PTEN expression in non-small cell lung cancer could be related to promoter methylation. , 2002, Clinical cancer research : an official journal of the American Association for Cancer Research.

[41]  R. Brezinschek,et al.  Mutation analysis of the PTEN/MMAC1 gene in lung cancer , 1998, Oncogene.