Antitumor Activity of SNX-2112, a Synthetic Heat Shock Protein-90 Inhibitor, in MET-Amplified Tumor Cells with or without Resistance to Selective MET Inhibition
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A. Olshen | A. Viale | N. Rosen | D. Solit | J. Christensen | M. Weiser | Z. Zeng | M. Mittlboeck | D. Líška | Ching-Tung Chen | T. Bachleitner-Hofmann | Mark Y. Sun
[1] U. McDermott,et al. Acquired resistance of non-small cell lung cancer cells to MET kinase inhibition is mediated by a switch to epidermal growth factor receptor dependency. , 2010, Cancer research.
[2] M. Ratain,et al. Clinical activity observed in a phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[3] Qing‐Yu He,et al. Transcriptomic and proteomic approach to studying SNX‐2112‐induced K562 cells apoptosis and anti‐leukemia activity in K562‐NOD/SCID mice , 2009, FEBS letters.
[4] M. Shah,et al. Assessment of two dosing schedules of GSK1363089 (GSK089), a dual MET/VEGFR2 inhibitor, in metastatic gastric cancer (GC): Interim results of a multicenter phase II study. , 2009, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.
[5] J. Veal,et al. Targeting of multiple signaling pathways by the Hsp90 inhibitor SNX-2112 in EGFR resistance models as a single agent or in combination with erlotinib. , 2009, Oncology research.
[6] Hiroshi Yasui,et al. SNX-2112, a selective Hsp90 inhibitor, potently inhibits tumor cell growth, angiogenesis, and osteoclastogenesis in multiple myeloma and other hematologic tumors by abrogating signaling via Akt and ERK. , 2009, Blood.
[7] P. Bunn,et al. Fibroblast Growth Factor (FGF) and FGF Receptor-Mediated Autocrine Signaling in Non-Small-Cell Lung Cancer Cells , 2009, Molecular Pharmacology.
[8] U. Banerji,et al. Heat Shock Protein 90 as a Drug Target: Some Like It Hot , 2009, Clinical Cancer Research.
[9] 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.
[10] M. Meyerson,et al. Hsp90 inhibition suppresses mutant EGFR-T790M signaling and overcomes kinase inhibitor resistance. , 2008, Cancer research.
[11] 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.
[12] Mithat Gonen,et al. Inhibition of Hsp90 down-regulates mutant epidermal growth factor receptor (EGFR) expression and sensitizes EGFR mutant tumors to paclitaxel. , 2008, Cancer research.
[13] Sarat Chandarlapaty,et al. SNX2112, a Synthetic Heat Shock Protein 90 Inhibitor, Has Potent Antitumor Activity against HER Kinase–Dependent Cancers , 2008, Clinical Cancer Research.
[14] Shinji Yamazaki,et al. Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma , 2007, Molecular Cancer Therapeutics.
[15] 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.
[16] Paul Workman,et al. Drugging the Cancer Chaperone HSP90 , 2007, Annals of the New York Academy of Sciences.
[17] L. Neckers,et al. Low Dose Geldanamycin Inhibits Hepatocyte Growth Factor- and Hypoxia-Stimulated Invasion of Cancer Cells , 2007, Cell cycle.
[18] Joon-Oh Park,et al. MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling , 2007, Science.
[19] 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.
[20] M. Weiser,et al. Molecular co-expression of the c-Met oncogene and hepatocyte growth factor in primary colon cancer predicts tumor stage and clinical outcome. , 2007, Cancer letters.
[21] M. Weiser,et al. Novel xenograft model expressing human hepatocyte growth factor shows ligand-dependent growth of c-Met–expressing tumors , 2007, Molecular Cancer Therapeutics.
[22] N. Kohl,et al. Lung cancer cell lines harboring MET gene amplification are dependent on Met for growth and survival. , 2007, Cancer research.
[23] 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.
[24] E. Sausville,et al. Geldanamycin derivative inhibition of HGF/SF-mediated Met tyrosine kinase receptor-dependent urokinase-plasminogen activation. , 2005, Bioorganic & medicinal chemistry.
[25] A. Lowell,et al. Epidermal growth factor receptors harboring kinase domain mutations associate with the heat shock protein 90 chaperone and are destabilized following exposure to geldanamycins. , 2005, Cancer research.
[26] E. Sausville,et al. Geldanamycins exquisitely inhibit HGF/SF-mediated tumor cell invasion , 2005, Oncogene.
[27] W. Birchmeier,et al. Met, metastasis, motility and more , 2003, Nature Reviews Molecular Cell Biology.
[28] J. Christensen,et al. A selective small molecule inhibitor of c-Met kinase inhibits c-Met-dependent phenotypes in vitro and exhibits cytoreductive antitumor activity in vivo. , 2003, Cancer research.
[29] N. Rosen,et al. Akt Forms an Intracellular Complex with Heat Shock Protein 90 (Hsp90) and Cdc37 and Is Destabilized by Inhibitors of Hsp90 Function* , 2002, The Journal of Biological Chemistry.
[30] C. Cordon-Cardo,et al. 17-Allylamino-17-demethoxygeldanamycin induces the degradation of androgen receptor and HER-2/neu and inhibits the growth of prostate cancer xenografts. , 2002, Clinical cancer research : an official journal of the American Association for Cancer Research.
[31] N. Rosen,et al. Ansamycin antibiotics inhibit Akt activation and cyclin D expression in breast cancer cells that overexpress HER2 , 2002, Oncogene.
[32] O. Brison,et al. Regulation of FGF-3 Gene Expression in Tumorigenic and Non-tumorigenic Clones of a Human Colon Carcinoma Cell Line* , 2000, The Journal of Biological Chemistry.
[33] J. Foidart,et al. Progression in MCF-7 breast cancer cell tumorigenicity: compared effect of FGF-3 and FGF-4 , 2000, Breast Cancer Research and Treatment.
[34] E. Sausville,et al. The geldanamycins are potent inhibitors of the hepatocyte growth factor/scatter factor-met-urokinase plasminogen activator-plasmin proteolytic network. , 2000, Cancer research.
[35] J. Foidart,et al. FGF-3 and FGF-4 elicit distinct oncogenic properties in mouse mammary myoepithelial cells , 1998, Oncogene.
[36] L. Neckers,et al. Destabilization of Raf-1 by geldanamycin leads to disruption of the Raf-1-MEK-mitogen-activated protein kinase signalling pathway , 1996, Molecular and cellular biology.
[37] C. MacArthur,et al. Receptor Specificity of the Fibroblast Growth Factor Family* , 1996, The Journal of Biological Chemistry.
[38] A. Hajitou,et al. Fibroblast growth factor 3 is tumorigenic for mouse mammary cells orthotopically implanted in nude mice , 1995, International journal of cancer.
[39] O. Brison,et al. The proto-oncogene FGF-3 is constitutively expressed in tumorigenic, but not in non-tumorigenic, clones of a human colon carcinoma cell line. , 1995, Oncogene.
[40] L. Neckers,et al. Inhibition of heat shock protein HSP90-pp60v-src heteroprotein complex formation by benzoquinone ansamycins: essential role for stress proteins in oncogenic transformation. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[41] C. Cooper,et al. Tyrosine kinase receptor indistinguishable from the c-met protein , 1989, Nature.
[42] M. Braun,et al. Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors. , 1987, Proceedings of the National Academy of Sciences of the United States of America.