Synthetic lethal screening reveals FGFR as one of the combinatorial targets to overcome resistance to Met-targeted therapy

[1]  J. M. Lee,et al.  Cbl-independent degradation of Met: ways to avoid agonism of bivalent Met-targeting antibody , 2014, Oncogene.

[2]  Ryan J. Jacobs,et al.  Alternative Signaling Pathways as Potential Therapeutic Targets for Overcoming EGFR and c-Met Inhibitor Resistance in Non-Small Cell Lung Cancer , 2013, PloS one.

[3]  G. Scagliotti,et al.  The emerging role of MET/HGF inhibitors in oncology. , 2013, Cancer treatment reviews.

[4]  P. Johnston,et al.  Cancer drug resistance: an evolving paradigm , 2013, Nature Reviews Cancer.

[5]  D. Wheeler,et al.  Targeting AKT with the allosteric AKT inhibitor MK-2206 in non-small cell lung cancer cells with acquired resistance to cetuximab , 2013, Cancer biology & therapy.

[6]  Katherine R. Singleton,et al.  A Receptor Tyrosine Kinase Network Composed of Fibroblast Growth Factor Receptors, Epidermal Growth Factor Receptor, v-erb-b2 Erythroblastic Leukemia Viral Oncogene Homolog 2, and Hepatocyte Growth Factor Receptor Drives Growth and Survival of Head and Neck Squamous Carcinoma Cell Lines , 2013, Molecular Pharmacology.

[7]  A. Bardelli,et al.  Tivantinib (ARQ197) Displays Cytotoxic Activity That Is Independent of Its Ability to Bind MET , 2013, Clinical Cancer Research.

[8]  L. Landi,et al.  Targeting c-MET in the battle against advanced nonsmall-cell lung cancer , 2013, Current opinion in oncology.

[9]  J. Sculier Nonsmall cell lung cancer , 2013, European Respiratory Review.

[10]  Caicun Zhou,et al.  Association of integrin beta1 and c-MET in mediating EGFR TKI gefitinib resistance in non-small cell lung cancer , 2013, Cancer Cell International.

[11]  Travis J Cohoon,et al.  Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models. , 2013, Cancer cell.

[12]  D. Nam,et al.  A new anti-c-met antibody selected by a mechanism-based dual-screening method: Therapeutic potential in cancer , 2012, Molecules and cells.

[13]  Rebeccah L. Brown,et al.  Cabozantinib for the Treatment of Advanced Medullary Thyroid Cancer , 2012, Advances in Therapy.

[14]  Jeffrey A. Porter,et al.  Rescue screens with secreted proteins reveal compensatory potential of receptor tyrosine kinases in driving cancer growth. , 2012, Cancer discovery.

[15]  S. Estrem,et al.  Reactivation of Mitogen-activated Protein Kinase (MAPK) Pathway by FGF Receptor 3 (FGFR3)/Ras Mediates Resistance to Vemurafenib in Human B-RAF V600E Mutant Melanoma* , 2012, The Journal of Biological Chemistry.

[16]  Yongjun Zhao,et al.  A Novel SND1-BRAF Fusion Confers Resistance to c-Met Inhibitor PF-04217903 in GTL16 Cells though MAPK Activation , 2012, PloS one.

[17]  H. Lee,et al.  MET in gastric carcinomas: comparison between protein expression and gene copy number and impact on clinical outcome , 2012, British Journal of Cancer.

[18]  D. Bottaro,et al.  Targeting the HGF/Met signaling pathway in cancer therapy , 2012, Expert opinion on therapeutic targets.

[19]  Andrew L. Kung,et al.  Autocrine activation of the MET receptor tyrosine kinase in acute myeloid leukemia , 2012, Nature Medicine.

[20]  R. Bernards,et al.  Unresponsiveness of colon cancer to BRAF(V600E) inhibition through feedback activation of EGFR , 2012, Nature.

[21]  Jeffrey W. Clark,et al.  MET amplification identifies a small and aggressive subgroup of esophagogastric adenocarcinoma with evidence of responsiveness to crizotinib. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[22]  R. Salgia,et al.  Role of MetMAb (OA-5D5) in c-MET active lung malignancies , 2011, Expert opinion on biological therapy.

[23]  Pascal Furet,et al.  Discovery of 3-(2,6-dichloro-3,5-dimethoxy-phenyl)-1-{6-[4-(4-ethyl-piperazin-1-yl)-phenylamino]-pyrimidin-4-yl}-1-methyl-urea (NVP-BGJ398), a potent and selective inhibitor of the fibroblast growth factor receptor family of receptor tyrosine kinase. , 2011, Journal of medicinal chemistry.

[24]  S. Hilsenbeck,et al.  β1 integrin mediates an alternative survival pathway in breast cancer cells resistant to lapatinib , 2011, Breast Cancer Research.

[25]  L. Sequist,et al.  Randomized phase II study of erlotinib plus tivantinib versus erlotinib plus placebo in previously treated non-small-cell lung cancer. , 2011, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[26]  Joseph Schoepfer,et al.  A drug resistance screen using a selective MET inhibitor reveals a spectrum of mutations that partially overlap with activating mutations found in cancer patients. , 2011, Cancer research.

[27]  Jeffrey W. Clark,et al.  Activity of crizotinib (PF02341066), a dual mesenchymal-epithelial transition (MET) and anaplastic lymphoma kinase (ALK) inhibitor, in a non-small cell lung cancer patient with de novo MET amplification. , 2011, Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer.

[28]  P. Comoglio,et al.  MET and KRAS gene amplification mediates acquired resistance to MET tyrosine kinase inhibitors. , 2010, Cancer research.

[29]  Karthik Devarajan,et al.  Synthetic Lethal Screen of an EGFR-Centered Network to Improve Targeted Therapies , 2010, Science Signaling.

[30]  R. Gillies,et al.  Molecular imaging and targeted therapies. , 2010, Biochemical pharmacology.

[31]  G. V. Vande Woude,et al.  MET kinase inhibitor SGX523 synergizes with epidermal growth factor receptor inhibitor erlotinib in a hepatocyte growth factor-dependent fashion to suppress carcinoma growth. , 2010, Cancer research.

[32]  T. Kuwana,et al.  Diminished Sensitivity of Chronic Lymphocytic Leukemia Cells to ABT-737 and ABT-263 Due to Albumin Binding in Blood , 2010, Clinical Cancer Research.

[33]  P. Majumder,et al.  MK-2206, an Allosteric Akt Inhibitor, Enhances Antitumor Efficacy by Standard Chemotherapeutic Agents or Molecular Targeted Drugs In vitro and In vivo , 2010, Molecular Cancer Therapeutics.

[34]  L. Trusolino,et al.  Activation of HER family members in gastric carcinoma cells mediates resistance to MET inhibition , 2010, Molecular Cancer.

[35]  D. Schiff,et al.  XL-184, a MET, VEGFR-2 and RET kinase inhibitor for the treatment of thyroid cancer, glioblastoma multiforme and NSCLC. , 2010, IDrugs : the investigational drugs journal.

[36]  Luca Toschi,et al.  Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC. , 2010, Cancer cell.

[37]  J. Mackey,et al.  Beta1-integrin circumvents the antiproliferative effects of trastuzumab in human epidermal growth factor receptor-2-positive breast cancer. , 2009, Cancer research.

[38]  Nathanael Gray,et al.  Factors underlying sensitivity of cancers to small-molecule kinase inhibitors , 2009, Nature Reviews Drug Discovery.

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

[40]  N. Rosen,et al.  HER kinase activation confers resistance to MET tyrosine kinase inhibition in MET oncogene-addicted gastric cancer cells , 2008, Molecular Cancer Therapeutics.

[41]  P. Bonnier,et al.  Poor prognosis in breast carcinomas correlates with increased expression of targetable CD146 and c-Met and with proteomic basal-like phenotype. , 2007, Human pathology.

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

[43]  B. Paulweber,et al.  Integrin alpha-2 and beta-3 gene polymorphisms and breast cancer risk , 2006, Breast Cancer Research and Treatment.

[44]  Gayatry Mohapatra,et al.  Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752 , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[45]  Y. Yen,et al.  Fibroblast growth factor receptor 3 inhibition by short hairpin RNAs leads to apoptosis in multiple myeloma , 2005, Molecular Cancer Therapeutics.

[46]  D. Wickramasinghe,et al.  Met Activation and Receptor Dimerization in Cancer: A Role for the Sema Domain , 2005, Cell cycle.

[47]  W. Birchmeier,et al.  Met, metastasis, motility and more , 2003, Nature Reviews Molecular Cell Biology.

[48]  Kathleen R. Lamborn,et al.  Cilengitide Targeting of αvβ3 Integrin Receptor Synergizes with Radioimmunotherapy to Increase Efficacy and Apoptosis in Breast Cancer Xenografts , 2002 .

[49]  K. M. Nicholson,et al.  The protein kinase B/Akt signalling pathway in human malignancy. , 2002, Cellular signalling.

[50]  G. V. Vande Woude,et al.  Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kinase/Akt and mitogen-activated protein kinase pathways. , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[51]  A. Chambers,et al.  Osteopontin‐induced, integrin‐dependent migration of human mammary epithelial cells involves activation of the hepatocyte growth factor receptor (Met) , 2000, Journal of cellular biochemistry.

[52]  Horst Kessler,et al.  N-methylated cyclic RGD peptides as highly active and selective αvβ3 integrin antagonists , 1999 .

[53]  S. Hubbard,et al.  Crystal structure of an angiogenesis inhibitor bound to the FGF receptor tyrosine kinase domain , 1998, The EMBO journal.

[54]  J. L. Burn Was it a drug? , 1972, British medical journal.

[55]  K. Lamborn,et al.  Cilengitide targeting of alpha(v)beta(3) integrin receptor synergizes with radioimmunotherapy to increase efficacy and apoptosis in breast cancer xenografts. , 2002, Cancer research.

[56]  S. Goodman,et al.  N-Methylated cyclic RGD peptides as highly active and selective alpha(V)beta(3) integrin antagonists. , 1999, Journal of medicinal chemistry.

[57]  G. Curley,et al.  Integrin antagonists , 1999, Cellular and Molecular Life Sciences CMLS.