Higher levels of c-Met expression and phosphorylation identify cell lines with increased sensitivity to AMG-458, a novel selective c-Met inhibitor with radiosensitizing effects

International Journal of Radiation Oncology Biology Physics

Volumn 84, Issue 4, 2012, Pages

  Li, Bo ^a   Torossian, Artour ^a   Sun, Yunguang ^b   Du, Ruihong ^a   Dicker, Adam P ^a   Lu, Bo ^a,b  

^a VANDERBILT INGRAM CANCER CENTER   (United States)

^b THOMAS JEFFERSON UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CELL DEATH; PHOSPHORYLATION; RADIOTHERAPY; TISSUE;

C-MET INHIBITORS; CLONOGENIC SURVIVAL ASSAYS; COMBINATION TREATMENTS; HEPATOCYTE GROWTH FACTOR; METHODS AND MATERIALS; MOLECULAR THERAPY; NON SMALL CELL LUNG CANCER; SMALL INTERFERING RNA;

CELL CULTURE;

AMG 458; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN INHIBITOR; PROTEIN KINASE B; SCATTER FACTOR RECEPTOR; UNCLASSIFIED DRUG; 1 (2 HYDROXY 2 METHYLPROPYL) N (5 (7 METHOXYQUINOLIN 4 YLOXY)PYRIDIN 2 YL) 5 METHYL 3 OXO 2 PHENYL 2,3 DIHYDRO 1H PYRAZOLE 4 CARBOXAMIDE; 1-(2-HYDROXY-2-METHYLPROPYL)-N-(5-(7-METHOXYQUINOLIN-4-YLOXY)PYRIDIN-2-YL)-5-METHYL-3-OXO-2-PHENYL-2,3-DIHYDRO-1H-PYRAZOLE-4-CARBOXAMIDE; AMINOPYRIDINE DERIVATIVE; PYRAZOLE DERIVATIVE; RADIOSENSITIZING AGENT; TUMOR PROTEIN;

APOPTOSIS; ARTICLE; CANCER CELL CULTURE; CELL SURVIVAL; CONTROLLED STUDY; HUMAN; HUMAN CELL; LUNG NON SMALL CELL CANCER; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN PHOSPHORYLATION; RADIOSENSITIVITY; RADIOSENSITIZATION; SIGNAL TRANSDUCTION; DRUG ANTAGONISM; DRUG EFFECT; DRUG SCREENING; LUNG TUMOR; METABOLISM; METHODOLOGY; PATHOLOGY; PHOSPHORYLATION; RADIATION DOSE; RADIATION EXPOSURE; TUMOR CELL LINE;

AMINOPYRIDINES; APOPTOSIS; CARCINOMA, NON-SMALL-CELL LUNG; CELL LINE, TUMOR; CELL SURVIVAL; DRUG SCREENING ASSAYS, ANTITUMOR; HUMANS; LUNG NEOPLASMS; NEOPLASM PROTEINS; PHOSPHORYLATION; PROTO-ONCOGENE PROTEINS C-MET; PYRAZOLES; RADIATION TOLERANCE; RADIATION-SENSITIZING AGENTS;

EID: 84872045438     PISSN: 03603016     EISSN: 1879355X     Source Type: Journal    
DOI: 10.1016/j.ijrobp.2012.06.025     Document Type: Article

References (18)

1. Birchmeier C, Birchmeier W, Gherardi E, et al. Met, metastasis, motility and more. Nat Rev Mol Cell Biol 2003; 4: 915-925.
2. Zeng Q, Chen S, You Z, et al. Hepatocyte growth factor inhibits anoikis in head and neck squamous cell carcinoma cells by activation of ERK and Akt signaling independent of NFkappa B. J Biol Chem 2002; 277: 25203-25208.
3. Ma PC, Jagadeeswaran R, Jagadeesh S, et al. Functional expression and mutations of c-Met and its therapeutic inhibition with SU11274 and small interfering RNA in non-small cell lung cancer. Cancer Res 2005; 65: 1479-1488.
4. Jiang W, Hiscox S, Matsumoto K, et al. Hepatocyte growth factor/scatter factor, its molecular, cellular and clinical implications in cancer. Crit Rev Oncol Hematol 1999; 29: 209-248.
5. Bean J, Brennan C, Shih JY, et al. MET amplification occurs with or without T790M mutations in EGFR mutant lung tumors with acquired resistance to gefitinib or erlotinib. Proc Natl Acad Sci U S A 2007; 104: 20932-20937.
6. Christensen JG, Schreck R, Burrows J, et al. A selective small molecule inhibitor of c-Met kinase inhibits c-Met-dependent pheno-types in vitro and exhibits cytoreductive antitumor activity in vivo. Cancer Res 2003; 63: 7345-7355.
7. Smolen GA, Sordella R, Muir B, et al. Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752. Proc Natl Acad Sci U S A 2006; 103: 2316-2321.
8. Canadas I, Rojo F, Arumi-Uria M, et al. C-MET as a new therapeutic target for the development of novel anticancer drugs. Clin Transl Oncol 2010; 12: 253-260.
9. Paez JG, Janne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 2004; 304: 1497-1500.
10. Lutterbach B, Zeng Q, Davis LJ, et al. Lung cancer cell lines harboring MET gene amplification are dependent on Met for growth and survival. Cancer Res 2007; 67: 2081-2088.
11. Bianco C, Tortora G, Bianco R, et al. Enhancement of antitumor activity of ionizing radiation by combined treatment with the selective epidermal growth factor receptor-tyrosine kinase inhibitor ZD1839 (Iressa). Clin Cancer Res 2002; 8: 3250-3258.
12. Guo A, Villen J, Kornhauser J, et al. Signaling networks assembled by oncogenic EGFR and c-Met. Proc Natl Acad Sci U S A 2008; 105: 692-697.
13. Xiao GH, Jeffers M, Bellacosa A, et al. Anti-apoptotic signaling by hepatocyte growth factor/Met via the phosphatidylinositol 3-kin-ase/Akt and mitogen-activated protein kinase pathways. Proc Natl Acad Sci U S A 2001; 98: 247-252.
14. McCubrey JA, Steelman LS, Chappell WH, et al. Roles of the Raf/MEK/ERK pathway in cell growth, malignant transformation and drug resistance. Biochim Biophys Acta 2007; 1773: 1263-1284.
15. Stommel JM, Kimmelman AC, Ying H, et al. Coactivation of receptor tyrosine kinases affects the response of tumor cells to targeted therapies. Science 2007; 318: 287-290.
16. Qi J, McTigue MA, Rogers A, et al. Multiple mutations and bypass mechanisms can contribute to development of acquired resistance to MET inhibitors. Cancer Res 2011; 71: 1081-1091.
17. Schmidt C. Why do tumors become resistant to antiangiogenesis drugs? J Natl Cancer Inst 2009; 101: 1530-1532.
18. Spigel DR, Ervin TJ, Ramlau R, et al. Final efficacy results from OAM4558g, a randomized phase II study evaluating MetMAb or placebo in combination with erlotinib in advanced NSCLC [Abstract]. J Clin Oncol 2011; 29(suppl l):7505.