Agents in the preclinical development stage for non-small cell lung cancer

References

• Torre LA, Bray F, Siegel RL, et al. Global cancer statistics, 2012. CA Cancer J Clin 2015;65(2):87-108
   PubMed Web of Science ®Google Scholar
• Rossi A, Maione P, Sacco PC, et al. ALK inhibitors and advanced non-small cell lung cancer (review). Int J Oncol 2014;45(2):499-508
   PubMed Web of Science ®Google Scholar
• Peters S, Adjei AA, Gridelli C, et al. Metastatic non-small-cell lung cancer (NSCLC): ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up. Ann Oncol 2012;23(Suppl 7):vii56-64
   PubMed Web of Science ®Google Scholar
• Mendelsohn J. Targeting the epidermal growth factor receptor for cancer therapy. J Clin Oncol 2002;20:1S-3S
   PubMed Web of Science ®Google Scholar
• Pirker R, Pereira JR, Szczesna A, et al. Cetuximab plus Chemotherapy in patients with advanced non-small cell lung cancer (FLEX): an open-label randomized phase III trial. Lancet 2009;373:1525-31
   PubMed Web of Science ®Google Scholar
• Thatcher N, Hirsh F, Luft AV, et al. SQUIRE: a randomized, multicenter, open-label, phase III trial study of gemcitabine-cisplatin (GEM-CIS) chemotherapy plus necitumumab (IMC-11F8/LY3012211) versus GEM-CIS alone in the first line treatment of patients with stage IV squamous non-small cell lung cancer (sq-NSCLC). Presented as an abstract and oral presentation at the 50th Annual Meeting of the ASCO; 2014. abstract 8008
   Google Scholar
• Yu HA, Arcila ME, Rekhtman N, et al. Analysis of tumor specimens at the time of acquired resistance to EGFR-TKI therapy in 155 patients with EGFR-mutant lung cancers. Clin Cancer Res 2013;19:2240-7
   PubMed Web of Science ®Google Scholar
• Yun CH, Mengwasser KE, Toms AV, et al. The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP. Proc Natl Acad Sci USA 2008;105:2070-5
   PubMed Web of Science ®Google Scholar
• Miller VA, Hirsh V, Cadranel J, et al. Afatinib placebo for patients with advanced, metastatic non–small cell lung cancer after failure of erlotinib, gefitinib, or both, and one or two lines of chemotherapy (LUX-Lung 1): a phase 2b/3 randomized trial. Lancet Oncol 2012;13:528-38
   PubMed Web of Science ®Google Scholar
• Sequist LV, Besse B, Lynch TJ, et al. Neratinib, an irreversible pan-ErbB receptor tyrosine kinase inhibitor: results of a phase II trial in patients with advanced non-small-cell lung cancer. J Clin Oncol 2010;28:3076-83
   PubMed Web of Science ®Google Scholar
• Pao W, Miller VA, Politi KA, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005;2:e73
   PubMed Web of Science ®Google Scholar
• Ho-June L, Schaefer G, P Heffron T, et al. Non covalent Wild-type–Sparing Inhibitors of EGFR T790M. Cancer Discov 2012;3(2):168-81
   Google Scholar
• Whitesell L, Lindquist SL. HSP90 and the chaperoning of cancer. Nat Rev Cancer 2005;5(10):761-72
   PubMed Web of Science ®Google Scholar
• Ono N, Yamazaki T, Tsukaguchi T, et al. Enhanced antitumor activity of erlotinib in combination with the Hsp90 inhibitor CH5164840 against non-small-cell lung cancer. Cancer Sci 2013;104(10):1346-52
   PubMed Web of Science ®Google Scholar
• Chiarle R, Voena C, Ambrogio C, et al. The anaplastic lymphoma kinase in the pathogenesis of cancer. Nat Rev Cancer 2008;8:11-23
   PubMed Web of Science ®Google Scholar
• Barlesi F, Blons H, Beau-Faller M, et al. Biomarkers (BM) France: results of routine EGFR, HER2, KRAS, BRAF, PI3KCA mutations detection and EML4-ALK gene fusion assessment on the first 10,000 non-small cell lung cancer (NSCLC) patients (pts). J Clin Oncol 2013;31:8000
   Web of Science ®Google Scholar
• Johnson BE, Kris MG, Berry LD, et al. A multicenter effort to identify driver mutations and employ targeted therapy in patients with lung adenocarcinomas: The Lung Cancer Mutation Consortium (LCMC). J Clin Oncol 2013;31:8019
   Web of Science ®Google Scholar
• Shaw AT, Kim DW, Nakagawa K, et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N Engl J Med 2013;368:2385-94
   PubMed Web of Science ®Google Scholar
• Mok T, Kim DW, Wu YL, et al. First-line crizotinib versus pemetrexed–cisplatin or pemetrexed–carboplatin in patients (pts) with advanced ALK-positive non-squamous non-small cell lung cancer (NSCLC), results of a Phase III study (PROFILE 1014). J Clin Oncol 2014;32(5s):Abstract 8002
   Google Scholar
• Kim DW, Mehra R, Tan DSW, et al. Ceritinib in advanced anaplastic lymphoma kinase (ALK)-rearranged (ALK+) non small cell lung cancer (NSCLC), Results of the ASCEND-1 trial. J Clin Oncol 2014;32(5s Suppl):Abstract 8003
   Google Scholar
• Choi YL, Soda M, Yamashita Y, et al. EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors. N Engl J Med 2010;363:1734-9
   PubMed Web of Science ®Google Scholar
• Pao W, Miller VA, Politi KA, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005;2:e73
   PubMed Web of Science ®Google Scholar
• Mori M, Ueno Y, Konagai S, et al. The Selective Anaplastic Lymphoma Receptor Tyrosine Kinase Inhibitor ASP3026 Induces Tumor Regression and Prolongs Survival in Non–Small Cell Lung Cancer Model Mice. Mol Cancer Ther 2014;13(2):329-40
   PubMed Web of Science ®Google Scholar
• Drew L, Cheng J, Engelman J, et al. Abstract 919: AZD3463, a novel ALK/IGF1R inhibitor, overcomes multiple mechanisms of acquired resistance to crizotinib. AACR. Cancer Res 2013;73(8 Suppl):Abstract nr 919
   Google Scholar
• Davies KD, Doebele RC. Molecular Pathways: ROS1 Fusion Proteins in Cancer. Clin Cancer Res 2013;19(15):4040-5
   PubMed Web of Science ®Google Scholar
• Davies KD, Le AT, Theodoro MF, et al. Identifying and targeting ROS1 gene fusions in non-small cell lung cancer. Clin Cancer Res 2012;18(17):4570-9
   PubMed Web of Science ®Google Scholar
• Takeuchi K, Soda M, Togashi Y, et al. RET, ROS1 and ALK fusions in lung cancer. Nat Med 2012;18(3):378-81
   PubMed Web of Science ®Google Scholar
• Ou S-HI, Bang Y-J, Camidge DR, et al. Efficacy and safety of crizotinib in patients with advanced ROS1-rearranged non-small cell lung cancer (NSCLC) [ASCO abstract 8032]. J Clin Oncol 2013;31:15 Suppl
   Google Scholar
• Awad MM, Katayama R, McTigue M, et al. Acquired resistance to crizotinib from a mutation in CD74-ROS1. N Engl J Med 2013;368(25):2395-401
   PubMed Web of Science ®Google Scholar
• Katayama R, Shaw AT, Khan TM, et al. Mechanisms of acquired crizotinib resistance in ALK-rearranged lung cancers. Sci Transl Med 2012;4(120):120ra17
   PubMed Web of Science ®Google Scholar
• Johnson TW, Richardson PF, Bailey S, et al. Discovery of (10R)-7-amino-12-fluoro-2,10,16-trimethyl-15-oxo-10,15,16,17tetrahydro2H8,4(metheno)pyrazolo[4,3h][2,5,11]benzoxadiazacyclotetradecine-3-carbonitrile (PF-06463922), a macrocyclic inhibitor of anaplastic lymphoma kinase (ALK) and c-ros oncogene 1 (ROS1) with preclinical brain exposure and broad spectrum potency against ALK-resistant mutations. J Med Chem 2014;57(11):4720-44
   PubMed Web of Science ®Google Scholar
• Zou HY, Li Q, Engstrom LD, et al. PF-06463922 is a potent and selective next-generation ROS1/ALK inhibitor capable of blocking crizotinib-resistant ROS1 mutations. PNAS 2015;112(11):3493-8
   PubMed Web of Science ®Google Scholar
• Onozato R, Kosaka T, Kuwano H, et al. Activation of MET by gene amplification or by splice mutations deleting the juxtamembrane domain in primary resected lung cancers. J Thorac Oncol 2009;4(1):5-11
   PubMed Web of Science ®Google Scholar
• Beau-Faller M, Ruppert AM, Voegeli AC, et al. MET gene copy number in non-small cell lung cancer: molecular analysis in a targeted tyrosine kinase inhibitor naive cohort. J Thorac Oncol 2008;3(4):331-9
   PubMed Web of Science ®Google Scholar
• 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 USA 2007;104(52):20932-7
   PubMed Web of Science ®Google Scholar
• Kobayashi S, Boggon TJ, Dayaram T, et al. EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. N Engl J Med 2005;352:786-92
   PubMed Web of Science ®Google Scholar
• Engelman JA, Zejnullahu K, Mitsudomi T, et al. MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science 2007;316:1039-43
   PubMed Web of Science ®Google Scholar
• 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 USA 2007;104:20932-7
   PubMed Web of Science ®Google Scholar
• Pao W, Miller VA, Politi KA, et al. Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain. PLoS Med 2005;2:e73
   PubMed Web of Science ®Google Scholar
• Lemke G, Rothlin CV. Immunobiology of the TAM receptors. Nat Rev Immunol 2008;8:327-36
   PubMed Web of Science ®Google Scholar
• Shankar SL, O’Guin K, Kim M, et al. Gas6/Axl signaling activates the phosphatidylinositol 3-kinase/Akt1 survival pathway to protect oligodendrocytes from tumor necrosis factor alpha-induced apoptosis. J Neurosci 2006;26:5638-48
   PubMed Web of Science ®Google Scholar
• Rho JK, Choi YJ, Kim SY, et al. MET and AXL Inhibitor NPS-1034 Exerts Efficacy against Lung Cancer Cells Resistant to EGFR Kinase Inhibitors Because of MET or AXL Activation. Cancer Res 2014;74(1):253-62
   PubMed Web of Science ®Google Scholar
• Somwar R, Erdjument-Bromage H, Larsson E, et al. Superoxide dismutase 1 (SOD1) is a target for a small molecule identified in a screen for inhibitors of the growth of lung adenocarcinoma cell lines. Proc Natl Acad Sci USA 2011;108(39):16375-80
   PubMed Web of Science ®Google Scholar
• Blum J, Fridovich I. Inactivation of glutathione peroxidise by superoxide radical. Arch Biochem Biophys 1985;240(2):500-8
   PubMed Web of Science ®Google Scholar
• Ichijo H, Nishida E, Irie K, et al. Induction of apoptosis by ASK1, a mammalian MAPKKK that activates SAPK/JNK and p38 signaling pathways. Science 1997;275(5296):90-4
   PubMed Web of Science ®Google Scholar
• Inoshita S, Takeda K, Hatai T, et al. Phosphorylation and inactivation of myeloid cell leukemia 1 by JNK in response to oxidative stress. J Biol Chem 2002;277(46):43730-4
   PubMed Web of Science ®Google Scholar
• Glasauer A, Sena LA, Diebold LP, et al. Targeting SOD1 reduces experimental non–small-cell lung cancer. J Clin Invest 2014;124(1):117-28
   PubMed Web of Science ®Google Scholar