88
Views
26
CrossRef citations to date
0
Altmetric
Review

Lung cancer therapeutics that target signaling pathways: an update

, &
Pages 631-645 | Published online: 09 Jan 2014

References

  • American Cancer Society. Cancer Facts & Figures 2009. American Cancer Society, Atlanta, GA, USA (2009).
  • National Cancer Institute. Non-small cell lung and bronchus cancer (invasive) survival rates, by race, sex, diagnosis year, state and age. SEER Cancer Statistics Review 1975–2004. National Cancer Institute, Bethesda, MD, USA (2008).
  • Greenlee R, Murray T, Bloden S, Wingo PA. Cancer statistics. CA Cancer J. Clin.50, 7–33 (2000).
  • Bunn PJ, Kelly K. New combinations in the treatment of lung cancer: a time for optimism. Chest117, 138–143 (2000).
  • Zhang Q, Feng W, Zhou H, Yan B. Advances in preclinical small molecules for the treatment of NSCLC. Expert Opin. Ther. Patents19, 741–751 (2009).
  • Carpenter G, Cohen S. Epidermal growth factor. J. Biol. Chem.265, 7709–7712 (1990).
  • Hanahan D, Weinberg RA. The hallmarks of cancer. Cell100, 57–70 (2000).
  • Ciardiello F, Tortora G. A novel approach in the treatment of cancer: targeting the epidermal growth factor receptor. Clin. Cancer Res.7, 2958–2970 (2001).
  • Gazdar A. Personalized medicine and inhibition of EGFR signaling in lung cancer. N. Engl. J. Med.361, 1018–1020 (2009).
  • Azim HA Jr, Ganti AK. Targeted therapy in advanced non-small cell lung cancer (NSCLC): where do we stand? Cancer Treat. Rev.32, 630–636 (2006).
  • Sequist L. Second-generation epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer. Oncologist12, 325–330 (2007).
  • Taron M, IchinoseY, Rossell R et al. Activating mutations in the tyrosine kinase domain of the epidermal growth factor receptor are associated with improved survival in gefitinib-treated chemorefractory lung adenocarcinomas. Clin. Cancer Res.11, 5878–5885 (2005).
  • Lynch TJ, Bell DW, Sordella R et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N. Engl. J. Med.350, 2129–2139 (2005).
  • Maemondo M, Inoue A, Kobayashi K et al. Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR. N. Engl. J. Med.362, 2380–2388 (2010).
  • Han S, Kim TY, Hwang PG et al. Predictive and prognostic impact of epidermal growth factor receptor mutation in non-small-cell lung cancer patients treated with gefitinib. J. Clin. Oncol.23, 5900–5909 (2005).
  • Engelman J, Jänne P. Mechanisms of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer. Clin. Cancer Res.14, 2895–2899 (2008).
  • Cappuzzo F, Marchetti A, Skokan M et al. Increased MET gene copy number negatively affects survival in surgically resected non-small-cell lung cancer patients. J. Clin. Oncol.27, 1667–1674 (2009).
  • Schiller JH, Akerley W, Brugger W et al. Results from ARQ 197–209: a global randomized placebo-controlled Phase II clinical trial of erlotinib plus ARQ 197 versus erlotinib plus placebo in previously treated EGFR inhibitor-naive patients with locally advanced or metastatic non-small-cell lung cancer (NSCLC). J. Clin. Oncol.28(18 Suppl.), abstract LBA 7502 (2010).
  • Sequist LV, Besse B, Lych 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.28, 3076–3083 (2010).
  • Riely G. Second-generation epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancer. J. Thorac. Oncol.3, 146–149 (2008).
  • Takezawa K, Okamoto I, Tanizaki J et al. Enhanced anticancer effect of the combination of BIBW2992 and thymidylate synthase-targeted agents in non-small cell lung cancer with the T790M mutation of epidermal growth factor receptor. Mol. Cancer Ther.9, 1647–1656 (2010).
  • Boyer MJ, Blackhall FH, Park K et al. Efficacy and safety of PF299804 versus erlotinib (E): a global, randomized Phase II trial in patients (pts) with advanced non-small cell lung cancer (NSCLC) after failure of chemotherapy (CT). J. Clin. Oncol.28(18 Suppl.), abstract LBA 7523 (2010).
  • Folkman J. Angiogenesis: an organizing principle for drug discovery? Nat. Rev. Drug Discov.6, 273–286 (2007).
  • Jain R. Normalization of tumor vasculature: an emerging concept in angiogenic therapy. Science307, 58–62 (2005).
  • Bergers G, Benjamin LE. Tumorigenesis and the angiogenic switch. Nat. Rev. Cancer3, 401–410 (2003).
  • Kalluri R. Basement membranes: structure, assembly and role in tumour angiogenesis. Nat. Rev. Cancer3, 422–433 (2003).
  • Fontanini G, Lucchi M, Vignati S et al. Angiogenesis as a prognostic indicator of survival in non-small cell lung carcinoma: a prospective study. J. Natl Cancer Inst.89, 881–886 (1997).
  • Hicklin D, Ellis LM. Role of the vascular endothelial growth factor pathway in tumor growth and angiogenesis. J. Clin. Oncol.23, 1011–1027 (2005).
  • Fong G, Rossant J, Gertsenstein M, Bretiman ML. Role of the Flt-1 receptor tyrosine kinase in regulating the assembly of vascular endothelium. Nature376, 66–70 (1995).
  • Ferrara N, Hillan KJ, Gerber HP, Novotny W. Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer. Nat. Rev. Drug Discov.3, 391–400 (2004).
  • Hurwitz H, Fehrenbacher L, Novotny W et al. Bevacizumab plus irinotecan, fluorouracil, and leucovorin for metastatic colorectal cancer. N. Engl. J. Med.350, 2335–2342 (2004).
  • Sandler A, Gray R, Perry MC et al. Paclitaxel–carboplatin alone or with bevacizumab for non-small-cell lung cancer. N. Engl. J. Med.355, 2542–2540 (2006).
  • Reck M, von Pawel J, Zatloukal P et al. Phase III trial of cisplatin plus gemcitabine with either placebo or bevacizumab as first-line therapy for nonsquamous non-small-cell lung cancer: AVAil. J. Clin. Oncol.27, 1227–1234 (2009).
  • Socinski MA, Novello S, Brahmer JR et al. Multicenter, Phase II trial of sunitinib in previously treated, advanced non-small-cell lung cancer. J. Clin. Oncol.26, 650–656 (2008).
  • Pal SK, Figlin RA, Reckamp K. Targeted therapies for non-small cell lung cancer: an evolving landscape. Mol. Cancer Ther.9, 1931–1944 (2010).
  • Amir E, Hughes S, Blackhall F et al. Targeting blood vessels for the treatment of non-small cell lung cancer. Curr. Cancer Drug Targets8, 392–403 (2008).
  • Blumenschein G Jr, Reckamp K, Stephenson GJ et al. Phase 1b study of motesanib, an oral angiogenesis inhibitor, in combination with carboplatin/paclitaxel and/or panitumumab for the treatment of advanced non-small cell lung cancer. Clin. Cancer Res.16, 279–290 (2010).
  • Goss G, Arnold A, Shepherd FA et al. Randomized, double-blind trial of carboplatin and paclitaxel with either daily oral cediranib or placebo in advanced non-small-cell lung cancer: NCIC clinical trials group BR24 study. J. Clin. Oncol.28, 49–55 (2010).
  • Schiller J, Larson T, Ou SI et al. Efficacy and safety of axitinib (AG-013736; AG) in patients with advanced non-small cell lung cancer (NSCLC): a Phase II trial. J. Clin. Oncol.25(18 Suppl.), abstract 7507 (2007).
  • Reck M. BIBF 1120 for the treatment of non-small cell lung cancer. Expert Opin. Investig. Drugs19, 789–794 (2010).
  • Head M, Jameson MB. The development of tumor vascular-disrupting agent ASA 404 (vadimezan, DMXAA): current status and future opportunities. Expert Opin. Investig. Drugs19, 295–304 (2010).
  • Pennell N, Lynch TJ Jr. Combined inhibition of the VEGFR and EGFR signaling pathways in the treatment of NSCLC. Oncologist14, 399–411 (2009).
  • Hainsworth J, Herbst R. A Phase III, multicenter, placebo-controlled, double-blind, randomized clinical trial to evaluate the efficacy of bevacizumab (Avastin) in combination with erlotinib (Tarceva) compared with erlotinib alone for treatment of advanced non-small cell lung cancer after failure of standard first-line chemotherapy. J. Thorac. Oncol.3, S302 (2008).
  • Clemmons D. Modifying IGF-1 activity: an approach to treat endocrine disorders, atherosclerosis, and cancer. Nat. Rev. Drug Discov.6, 821–833 (2007).
  • Gridelli C, Rossi A, Bareschino MA, Schettino C, Sacco PC, Maione P. The potential role of insulin-like growth factor receptor inhibitors in the treatment of advanced non-small cell lung cancer. Expert Opin. Investig. Drugs19, 631–639 (2010).
  • Yee D. Targeting insulin-like growth factor pathways. Br. J. Cancer94, 465–468 (2006).
  • Kulik G, Klippel A, Weber MJ. Antiapoptotic signaling by the insulin-like growth factor I receptor, phosphatidylinositol 3-kinase, and Akt. Mol. Cell Biol.17, 1595–1606 (1997).
  • Pandini G, Frasca F, Mineo R et al. Insulin/insulin-like growth factor I hybrid receptors have different biological characteristics depending on the insulin receptor isoform involved. J. Biol. Chem.277(42), 39684–39695 (2002).
  • Denley A, Cosgrove LJ, Booker GW et al. Molecular interactions of the IGF system. Cytokine Growth Factor Rev.16, 421–439 (2005).
  • Chao W, D’Amore PA. IGF2: epigenetic regulation and role in development and disease. Cytokine Growth Factor Rev.19, 111–120 (2008).
  • Yu, H, Spitz MR, Mistry J et al. Plasma levels of insulin-like growth factor-I and lung cancer risk: a case–control analysis. J. Natl Cancer Inst.91, 151–156 (1999).
  • Chang Y, Wang L, Liu D et al. Correlation between insulin-like growth factor-binding protein-3 promoter methylation and prognosis of patients with stage I non-small cell lung cancer. Clin. Cancer Res.8, 3669–3675 (2002).
  • Sordella R, Bell DW, Haber DA, Settleman J. Gefitinib-sensitizing EGFR mutations in lung cancer activate anti-apoptotic pathways. Science305, 1163–1167 (2004).
  • Cappuzzo F, Toschi L, Tallini G et al. Insulin-like growth factor receptor 1 (IGFR-1) is significantly associated with longer survival in non-small cell lung cancer patients treated with gefitinib. Ann. Oncol.17, 1120–1127 (2006).
  • Ludovini V, Bellezza G, Pistola L et al. High coexpression of both insulin-like growth factor receptor-1 (IGFR-1) and epidermal growth factor receptor (EGFR) is associated with shorter disease-free survival in resected non-small cell lung cancer patients. Ann. Oncol.20, 842–849 (2009).
  • Ullrich A, Gray A, Tam AW et al. Insulin-like growth factor I receptor primary structure: comparison with insulin receptor suggests structural determinants that define functional specificity. EMBO J.5, 2503–2512 (1986).
  • Garber K. IGF-1: old growth factor shines as new drug target. J. Natl Cancer Inst.97, 790–792 (2005).
  • Karp D, Pollak MN, Cohen RB et al. Safety, pharmacokinetics, and pharmacodynamics of the insulin-like growth factor type 1 receptor inhibitor figitumumab (CP-751,871) in combination with paclitaxel and carboplatin. J. Thorac. Oncol.4, 1397–1403 (2009).
  • Karp D, Paz-Ares LG, Novello S et al. Phase II study of the anti-insulin-like growth factor type 1 receptor antibody CP-751,871 in combination with paclitaxel and carboplatin in previously untreated, locally advanced, or metastatic non-small cell lung cancer. J. Clin. Oncol.27, 2516–2522 (2009).
  • Andrew S. PIK3CA: determining its role in cellular proliferation and ovarian cancer. Clin. Genet.56, 190–191 (1999).
  • Osaki M, Oshimura M, Ito H. PI3K–Akt pathway: its functions and alterations in human cancer. Apoptosis9, 667–676 (2004).
  • Kandasamy K, Srivastava RK. Role of the phosphatidylinositol 3’-kinase/PTEN/Akt kinase pathway in tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in non-small cell lung cancer cells. Cancer Res.62, 4929–4937 (2002).
  • Brognard J, Clark AS, Ni Y, Dennis PA. Akt/protein kinase B is constitutively active in non-small cell lung cancer cells and promotes cellular survival and resistance to chemotherapy and radiation. Cancer Res.61, 3986–3997 (2001).
  • Vignot S, Faivre S, Aguirre D, Raymond E. mTOR-targeted therapy of cancer with rapamycin derivatives. Ann. Oncol.24, 3348–3357 (2005).
  • Soria J, Shepherd FA, Douillard JY et al. Efficacy of everolimus (RAD001) in patients with advanced NSCLC previously treated with chemotherapy alone or with chemotherapy and EGFR inhibitors. Ann. Oncol.10, 1674–1681 (2009).
  • She Q, Solit DB, Ye Q et al. The BAD protein integrates survival signaling by EGFR/MAPK and PI3K/Akt kinase pathways in PTEN-deficient tumor cells. Cancer Cell8, 287–297 (2005).
  • Engelman J, Mukokhara T, Zejnullahu K et al. Allelic dilution obscures detection of a biologically signficant resistance mutation in EGFR-amplified lung cancer. J. Clin. Invest.116, 2695–2706 (2006).
  • Ferreira C, Epping M, Kruyt FA, Giaccone G. Apoptosis: target of cancer therapy. Clin. Cancer Res.8, 2024–2034 (2002).
  • Duiker E, Mom CH, de Jong S et al. The clinical trail of TRAIL. Eur. J. Cancer42, 2233–2240 (2006).
  • Ozoren N, El-Deiry WS. Defining characteristics of types I and II apoptotic cells in response to TRAIL. Neoplasia4, 551–557 (2002).
  • Kruyt F. TRAIL and cancer therapy. Cancer Lett.263, 14–25 (2008).
  • Fang F, Wang AP, Yang SF. Antitumor activity of a novel recombinant mutant human tumor necrosis factor-related apoptosis-inducing ligand. Acta Pharmacol. Sin.26, 1373–1381 (2005).
  • MacFarlane M, Kohlhaas SL, Sutcliffe MJ, Dyer MJ, Cohen GM. TRAIL receptor-selective mutants signal to apoptosis vial TRAIL-R1 in primary lymphoid malignancies. Cancer Res.65, 11265–11270 (2005).
  • Kelley R, Totpal K, Lindstrom SH et al. Receptor-selective mutants of apoptosis-inducing ligand 2/tumor necrosis factor-related apoptosis-inducing ligand reveal a greater contribution of death receptor (DR) 5 than DR4 to apoptosis signaling. J. Biol. Chem.280(3), 2205–2212 (2005).
  • Tur V, van der Sloot AM, Reis CR et al. DR4-selective tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) variants obtained by structure-based design. J. Biol. Chem.283, 20560–20568 (2008).
  • Yada A, Yazawa M, Ishida S et al. A novel humanized anti-human death receptor 5 antibody CS-1008 induces apoptosis in tumor cells without toxicity in hepatocytes. Ann. Oncol.19, 1060–1067 (2008).
  • Greco F, Bonomi P, Crawford J et al. Phase 2 study of mapatumumab, a fully human agonistic monoclonal antibody which targets and activates the TRAIL receptor-1, in patients with advanced non-small cell lung cancer. Lung Cancer61, 82–90 (2008).
  • Luster T, Carrell JA, McCormick K et al. Mapatumumab and lexatumumab induce apoptosis in TRAIL-R1 and TRAIL-R2 antibody-resistant NSCLC cell lines when treated in combination with bortezomib. Mol. Cancer Ther.8, 292–303 (2009).
  • Jin H, Yang R, Ross J et al. Cooperation of the agonistic DR5 antibody apomab with chemotherapy to inhibit orthotopic lung tumor growth and improve survival. Cancer Res.64, 4900–4905 (2008).
  • Takahashi T, Nau MM, Chiba I et al. P53: a frequent target for genetic abnormalities in lung cancer. Science246, 491–494 (1989).
  • Ferreira C, Span SW, Peters GH, Kruyt FA, Giaccone G. Chemotherapy triggers apoptosis in a caspase-8-dependent and mitochondria-controlled manner in the non-small cell lung cancer cell line NCI-H460. Cancer Res.60, 7133–7141 (2000).
  • Spierings D, de Vries EG, Timens W et al. Expression of TRAIL and TRAIL death receptors in stage III non-small cell lung cancer tumors. Clin. Cancer Res.9, 3397–3405 (2003).
  • Frese S, Brunner T, Gugger M, Uduehi A, Schmid RA. Enhancement of Apo2L/TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)-induced apoptosis in non-small cell lung cancer cell lines by chemotherapeutic agents without correlation to the expression level of cellular protease caspase-8 inhibitory protein. J. Thorac. Cardiovasc. Surg.123, 168–174 (2002).
  • Thorburn A, Behbakht K, Ford H. TRAIL receptor-targeted therapeutics: resistance mechanisms and strategies to avoid them. Drug Resist. Updates11, 17–24 (2008).
  • Scagliotti G. Proteasome inhibitors in lung cancer. Crit. Rev. Oncol. Hematol.58, 177–189 (2006).
  • Park S, Seol DW. Regulation of Akt by EGFR inhibitors, a possible mechanism of EGFR inhibitor-enhanced TRAIL-induced apoptosis. Biochem. Biophys. Res. Commun.295, 515–518 (2002).
  • Soria J, Smit EF, Khayat D et al. Phase Ib study of dulanermin (recombinant human Apo2L/TRAIL) in combination with paclitaxel, carboplatin and bevacizumab in patients with advanced non-small cell lung cancer. J. Clin. Oncol.28, 1527–1533 (2008).
  • Von Pawel J, Harvey H, Spigel DR et al. Randomized Phase II trial of mapatumumab, a TRAIL-R1 agonist monoclonal antibody, in combination with carboplatin and paclitaxel in patients with non-small-cell lung cancer (NSCLC). Presented at: 2010 Annual Oncology Meeting. Chicago, IL, USA, 4–8 June 2010 (Abstract LBA 7501).
  • LoRusso P, Hong D, Heath E et al. First-in-human study of AMG 655, a pro-apoptotic TRAIL receptor-2 agonist, in adult patients with advanced solid tumors. J. Clin. Oncol.25(Suppl. 18), 3534 (2007).
  • Stegehuis J, de Wilt LHAM, de Vries EGE, Groen HJ, de Jong S, Kruyt FAE. TRAIL receptor targeting therapies for non-small cell lung cancer: current status and perspectives. Drug Resist. Updates13, 2–15 (2010).
  • Soo E, Yip GW, Lwin ZM et al. Heat shock proteins as novel therapeutic targets in cancer. In Vivo22, 311–315 (2008).
  • Donnelly A, Blagg BSJ. Novobiocin and additional inhibitors of the Hsp90 C-terminal nucleotide-binding pocket. Curr. Med. Chem.15, 2702–2717 (2008).
  • Mahalingam D, Swords R, Carew JS et al. Targeting HSP90 for cancer therapy. Br. J. Cancer100, 1523–1529 (2009).
  • Uehara Y. Natural product origins of Hsp90 inhibitors. Curr. Cancer Drug Targets3, 325–330 (2003).
  • Conde R, Belak ZR, Nair M et al. Modulation of Hsf1 activity by novobiocin and geldanamycin. Biochem. Cell Biol.87, 845–851 (2009).
  • Chandarlapaty S, Sawai A, Ye Q et al. SNX2112, a synthetic heat shock protein 90 inhibitor, has potent antitumor activity against HER kinase-dependent cancers. Clin. Cancer Res.14, 240–248 (2008).
  • Radons J, Multhoff G. Immunostimulatory functions of membrane-bound and exported heat shock protein 70. Exerc. Immunol. Rev.11, 17–33 (2005).
  • Kallio P, Pongratz I, Gradin K, McGuire J, Poellinger L. Activation of hypoxia-inducible factor 1a: posttranscriptional regulation and conformational change by recruitment of the Arnt transcription factor. Proc. Natl Acad. Sci. USA94, 5667–5672 (1997).
  • Semenza G. Hypoxia-inducible factor 1: master regulator of O2 homeostasis. Curr. Opin. Genet. Dev.8, 588–594 (1998).
  • Elson D, Thurston G, Huang LE et al. Induction of hypervascularity without leakage or inflammation in transgenic mice overexpressing hypoxia-inducible factor-1a. Genes Dev.15, 2520–2532 (2001).
  • Brahimi-Horn M, Pouysségur J. The hypoxia-inducible factor and tumor progression along the angiogenic pathway. Int. Rev. Cytol.242, 157–213 (2005).
  • Jones P, Baylin SB. The epigenomics of cancer. Cell128, 683–692 (2007).
  • Luger K. Structure and dynamic behavior of nucleosomes. Curr. Opin. Genet. Dev.13, 127–135 (2003).
  • Lane A, Chabner BA. Histone deacetylase inhibitors in cancer therapy. J. Clin. Oncol.27, 5459–5468 (2009).
  • Strahl B, Allis CD. The language of covalent histone modifications. Nature403, 41–45 (2000).
  • Gregory P, Wagner K, Horz W. Histone acetylation and chromatin remodeling. Exp. Cell Res.265, 195–202 (2001).
  • Roth S, Denu JM, Allis CD. Histone acetyltransferases. Annu. Rev. Biochem.70, 81–120 (2001).
  • Gray S, Ekstrom TJ. The human histone deacetylase family. Exp. Cell Res.262, 75–83 (2001).
  • Zhang Y, Adachi M, Kawamura R et al. Bmf is a possible mediator in histone deacetylase inhibitors FK228 and CBHA-induced apoptosis. Cell Death Differ.13, 129–140 (2006).
  • Zhao Y, Tan J, Zhuang L et al. Inhibitors of histone deacetylases target the Rb-E2F1 pathway for apoptosis induction through activation of proapoptotic protein Bim. Proc. Natl Acad. Sci. USA102, 16090–16095 (2005).
  • Xu Y. Regulation of p53 responses by post-translational modifications. Cell Death Differ.10, 400–403 (2003).
  • Kim M, Kwon HJ, Lee YM et al. Histone deacetylases induce angiogenesis by negative regulation of tumor suppressor genes. Nat. Med.7, 437–543 (2001).
  • Fath D, Kong X, Liang D et al. Histone deacetylase inhibitors repress the transactivation potential of hypoxia-inducible factors independently of direct acetylation of HIF-α. J. Biol. Chem.281, 13612–13619 (2006).
  • Geng L, Cuneo KC, Fu A et al. Histone deacetylase (HDAC) inhibitor LBH589 increases duration of g-H2AX foci and confines HDAC4 to the cytoplasm in irradiated non-small cell lung cancer. Cancer Res.66, 11298–11304 (2006).
  • Edwards A, Li J, Atadja P et al. Effect of the histone deacetylase inhibitor LBH589 against epidermal growth factor receptor-dependent human lung cancer cells. Mol. Cancer Ther.6, 2515–2524 (2007).
  • Yagui-Beltrán A, He B, Raz D, Kim J, Jablons DM. Novel therapies targeting signaling pathways in lung cancer. Thorac. Surg. Clin.16, 379–396 (2006).
  • Bonnet D, Dick JE. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat. Med.3, 730–737 (1997).
  • O’Brien C, Pollett A, Gallinger S, Dick JE. A human colon cancer cell capable of initiating tumour growth in immunodeficient mice. Nature445, 106–110 (2007).
  • Ricci-Vitiani L, Lombardi DG, Pilozzi E et al. Identification and expansion of human colon-cancer-initiating cells. Nature445, 111–115 (2007).
  • Widelitz R. Wnt signaling through canonical and non-canonical pathways: recent progress. Growth Factors23, 111–116 (2005).
  • Akiyama T. Wnt/β-catenin signaling. Cytokine Growth Factor Rev.11, 273–282 (2000).
  • He B, You L, Uematsu K et al. A monoclonal antibody against Wnt-1 induces apoptosis in human cancer cells. Neoplasia6, 7–14 (2004).
  • Chen S, Guttridge DC, You Z. Wnt-1 signaling inhibits apoptosis by activating β-catenin/T cell factor-mediated transcription. J. Cell Biol.152, 87–96 (2001).
  • Uematsu K, He B, You L et al. Activation of the Wnt pathway in non small cell lung cancer: evidence of disheveled overexpression and transcriptional activity of β-catenin. Oncogene22, 7218–7221 (2003).
  • Kim J, You L, Xu Z et al. Wnt inhibitory factor inhibits lung cancer cell growth. J. Thorac. Cardiovasc. Surg.133, 733–737 (2007).
  • He B, Barg RN, You L et al. Wnt signaling in stem cells and non-small-cell lung cancer. Clin. Lung Cancer7, 54–60 (2005).
  • Lepourcelet M, Chen YN, France DS et al. Small-molecule antagonists of the oncogenic Tcf/β-catenin protein complex. Cancer Cell5, 91–102 (2004).
  • Emami K, Nguyen C, Ma H. A small molecule inhibitor of β-catenin/CREB-binding protein transcription. Proc. Natl Acad. Sci. USA101, 12682–12687 (2004).
  • Barker N, Clevers H. Mining the Wnt pathway for cancer therapeutics. Nat. Rev. Drug Discov.5, 997–1014 (2006).
  • Piyathilake C, Frost AR, Manne U et al. Differential expression of growth factors in squamous cell carcinoma and precancerous lesions of the lung. Clin. Cancer Res.8, 734–744 (2002).
  • Lonardo F, Dragnev KH, Freemantle SJ et al. Evidence for the epidermal growth factor receptor as a target for lung cancer prevention. Clin. Cancer Res.8, 54–60 (2002).
  • Volm M, Koomagi R, Mattern J. Prognostic value of p16INK4A expression in lung adenocarcinoma. Anticancer Res.18, 2309–2312 (1998).
  • Hall A, Dix BR, O’Carroll SJ et al. p53 status does not determine outcome of E1B 55-kilodalton mutant adenovirus lytic infection. J. Clin. Oncol.21, 4546–4552 (1998).
  • Von Hoff D, LoRusso PM, Rudin CM et al. Inhibition of the hedgehog pathway in advanced basal-cell carcinoma. N. Engl. J. Med.361, 1164–1172 (2009).
  • Soda M, Choi YL, Enomoto M et al. Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer. Nature448, 561–566 (2007).
  • Shaw A, Yeap BY, Mino-Kenudson M et al. Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4–ALK. J. Clin. Oncol.27, 4247–4253 (2009).
  • Inamura K, Takeuchi K, Togashi Y et al. EML4–ALK lung cancers are characterized by rare other mutations, a TTF-1 cell lineage, an acinar histology, and young onset. Mod. Pathol.22, 508–515 (2009).
  • Kwak E, Camidge DR, Clark J et al. Clinical activity observed in a Phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066. J. Clin. Oncol.27(15S), abstract 3509 (2009).
  • Bang Y, Kwak E, Shaw AT et al. Clinical activity of the oral ALK inhibitor PF-0234106 in ALK-positive patients with non-small-cell lung cancer. Presented at: 2010 Annual Oncology Meeting. Chicago, IL, USA, 4–8 June 2010 (Abstract 3).
  • Cronin M, Sangli C, Liu ML et al. Analytical validation of the Oncotype DX genomic diagnostic test for recurrence prognosis and therapeutic response prediction in node-negative, estrogen receptor-positive breast cancer. Clin. Chem.53, 1084–1091 (2007).
  • Raz D, Ray MR, Kim JY et al. A multigene assay is prognostic of survival in patients with early-stage lung adenocarcinoma. Clin. Cancer Res.14, 5565–5570 (2008).
  • Chen H, Yu SL, Chen CH et al. A five-gene signature and clinical outcome in non-small-cell lung cancer. N. Engl. J. Med.356, 11–20 (2007).
  • Skrzypski M, Jassem E, Taron M et al. Three-gene expression signature predicts survival in early-stage squamous cell carcinoma of the lung. Clin. Cancer Res.14, 4794–4799 (2008).
  • Kim IJ, Kim K, Kang HC, Jang SG, Park JG. DHPLC analysis of adenomatous polyposis coli (APC) mutations using ready-to-use APC plates: simple detection of multiple base pair deletion mutations. Genet. Test.12(2), 295–298 (2008).

Patents

  • Blaschuk OW, Byers S, Gour BJ. Compounds and methods for modulating β-catenin mediated gene expression. US6303576 (2001).
  • Moll J, Knapp S, Dalvit C, Trosset JY, Sundstrom M, Mantegani S. Interaction inhibitors of TCF-4 with β-catenin. Pharmacia Italia SPA: EP-1406889 (2004).
  • Kahn M, Eguch M, Moon SH, Chung JU, Jeong KW. Compounds useful for treatment of cancer, compositions containing the same, and methods of their use. Choongwae Pharma Corporation: US6762185 (2004).

Websites

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.