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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 陳青周 | |
dc.contributor.author | Yun-Chieh Lin | en |
dc.contributor.author | 林韵倢 | zh_TW |
dc.date.accessioned | 2021-06-13T01:03:24Z | - |
dc.date.available | 2016-10-07 | |
dc.date.copyright | 2011-10-07 | |
dc.date.issued | 2011 | |
dc.date.submitted | 2011-08-04 | |
dc.identifier.citation | Alao, J. P., Stavropoulou, A. V., et al. (2006). 'Histone deacetylase inhibitor, trichostatin A induces ubiquitin-dependent cyclin D1 degradation in MCF-7 breast cancer
cells.' Mol Cancer 5: 8. Allfrey, V. G., Faulkner, R., et al. (1964). 'Acetylation and Methylation of Histones and Their Possible Role in the Regulation of Rna Synthesis.' Proc Natl Acad Sci U S A 51: 786-794. Arriagada, R., Bergman, B., et al. (2004). 'Cisplatin-based adjuvant chemotherapy in patients with completely resected non-small-cell lung cancer.' N Engl J Med 350(4): 351-360. Arteaga, C. L. (2007). 'HER3 and mutant EGFR meet MET.' Nat Med 13(6): 675-677. Avizienyte, E., Ward, R. A., et al. (2008). 'Comparison of the EGFR resistance mutation profiles generated by EGFR-targeted tyrosine kinase inhibitors and the impact of drug combinations.' Biochem J 415(2): 197-206. Bali, P., George, P., et al. (2004). 'Superior activity of the combination of histone deacetylase inhibitor LAQ824 and the FLT-3 kinase inhibitor PKC412 against human acute myelogenous leukemia cells with mutant FLT-3.' Clin Cancer Res 10(15): 4991-4997. Bannister, A. J. and Kouzarides, T. (2011). 'Regulation of chromatin by histone modifications.' Cell Res 21(3): 381-395. Baselga, J. (2001). 'The EGFR as a target for anticancer therapy--focus on cetuximab.' Eur J Cancer 37 Suppl 4: S16-22. Baselga, J., Rischin, D., et al. (2002). 'Phase I safety, pharmacokinetic, and pharmacodynamic trial of ZD1839, a selective oral epidermal growth factor receptor tyrosine kinase inhibitor, in patients with five selected solid tumor types.' J Clin Oncol 20(21): 4292-4302. Bean, J., Brennan, C., et al. (2007). '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 104(52): 20932-20937. Bell, D. W., Gore, I., et al. (2005). 'Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR.' Nat Genet 37(12): 1315-1316. Bhalla, K. N. (2005). 'Epigenetic and chromatin modifiers as targeted therapy of hematologic malignancies.' J Clin Oncol 23(17): 3971-3993. Bolden, J. E., Peart, M. J., et al. (2006). 'Anticancer activities of histone deacetylase inhibitors.' Nat Rev Drug Discov 5(9): 769-784. Bruzzese, F., Leone, A., et al. (2010). 'HDAC inhibitor vorinostat enhances the antitumor effect of gefitinib in squamous cell carcinoma of head and neck by modulating ErbB receptor expression and reverting EMT.' J Cell Physiol. Cameron, E. E., Bachman, K. E., et al. (1999). 'Synergy of demethylation and histone deacetylase inhibition in the re-expression of genes silenced in cancer.' Nat Genet 21(1): 103-107. Carey, K. D., Garton, A. J., et al. (2006). 'Kinetic analysis of epidermal growth factor receptor somatic mutant proteins shows increased sensitivity to the epidermal growth factor receptor tyrosine kinase inhibitor, erlotinib.' Cancer Res 66(16): 8163-8171. Chang, C. Y., Shen, C. C., et al. (2011). 'Gefitinib induces apoptosis in human glioma cells by targeting Bad phosphorylation.' J Neurooncol. Chen, C. S., Wang, Y. C., et al. (2007). 'Histone deacetylase inhibitors sensitize prostate cancer cells to agents that produce DNA double-strand breaks by targeting Ku70 acetylation.' Cancer Res 67(11): 5318-5327. Chitale, D., Gong, Y., et al. (2009). 'An integrated genomic analysis of lung cancer reveals loss of DUSP4 in EGFR-mutant tumors.' Oncogene 28(31): 2773-2783. Cho, H. S. and Leahy, D. J. (2002). 'Structure of the extracellular region of HER3 reveals an interdomain tether.' Science 297(5585): 1330-1333. Chou, C. W. and Chen, C. C. (2008). 'HDAC inhibition upregulates the expression of angiostatic ADAMTS1.' FEBS Lett 582(29): 4059-4065. Chou, C. W., Wu, M. S., et al. (2011). 'HDAC inhibition decreases the expression of EGFR in colorectal cancer cells.' PLoS One 6(3): e18087. Ciardiello, F. and Tortora, G. (2008). 'EGFR antagonists in cancer treatment.' N Engl J Med 358(11): 1160-1174. Comoglio, P. M., Giordano, S., et al. (2008). 'Drug development of MET inhibitors: targeting oncogene addiction and expedience.' Nat Rev Drug Discov 7(6): 504-516. Costa, D. B., Halmos, B., et al. (2007). 'BIM mediates EGFR tyrosine kinase inhibitor-induced apoptosis in lung cancers with oncogenic EGFR mutations.' PLoS Med 4(10): 1669-1679; discussion 1680. Dankort, D., Jeyabalan, N., et al. (2001). 'Multiple ErbB-2/Neu Phosphorylation Sites Mediate Transformation through Distinct Effector Proteins.' J Biol Chem 276(42): 38921-38928. Das, C., Lucia, M. S., et al. (2009). 'CBP/p300-mediated acetylation of histone H3 on lysine 56.' Nature 459(7243): 113-117. Davies, H., Bignell, G. R., et al. (2002). 'Mutations of the BRAF gene in human cancer.' Nature 417(6892): 949-954. Deininger, M., Buchdunger, E., et al. (2005). 'The development of imatinib as a therapeutic agent for chronic myeloid leukemia.' Blood 105(7): 2640-2653. Deng, J., Shimamura, T., et al. (2007). 'Proapoptotic BH3-only BCL-2 family protein BIM connects death signaling from epidermal growth factor receptor inhibition to the mitochondrion.' Cancer Res 67(24): 11867-11875. Ding, L., Getz, G., et al. (2008). 'Somatic mutations affect key pathways in lung adenocarcinoma.' Nature 455(7216): 1069-1075. Du, Z., Song, J., et al. (2010). 'DNMT1 stability is regulated by proteins coordinating deubiquitination and acetylation-driven ubiquitination.' Sci Signal 3(146): ra80. Dziadziuszko, R., Camidge, D. R., et al. (2008). 'The insulin-like growth factor pathway in lung cancer.' J Thorac Oncol 3(8): 815-818. Eberhard, D. A., Johnson, B. E., et al. (2005). 'Mutations in the epidermal growth factor receptor and in KRAS are predictive and prognostic indicators in patients with non-small-cell lung cancer treated with chemotherapy alone and in combination with erlotinib.' J Clin Oncol 23(25): 5900-5909. Edwards, A., Li, J., et al. (2007). 'Effect of the histone deacetylase inhibitor LBH589 against epidermal growth factor receptor-dependent human lung cancer cells.' Mol Cancer Ther 6(9): 2515-2524. Ekstrand, A. J., Sugawa, N., et al. (1992). 'Amplified and rearranged epidermal growth factor receptor genes in human glioblastomas reveal deletions of sequences encoding portions of the N- and/or C-terminal tails.' Proc Natl Acad Sci U S A 89(10): 4309-4313. Engelman, J. A., Mukohara, T., et al. (2006). 'Allelic dilution obscures detection of a biologically significant resistance mutation in EGFR-amplified lung cancer.' J Clin Invest 116(10): 2695-2706. Engelman, J. A., Zejnullahu, K., et al. (2007). 'PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib.' Cancer Res 67(24): 11924-11932. Engelman, J. A., Zejnullahu, K., et al. (2007). 'MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling.' Science 316(5827): 1039-1043. Faber, A. C., Wong, K. K., et al. (2010). 'Differences underlying EGFR and HER2 oncogene addiction.' Cell Cycle 9(5): 851-852. Festuccia, C., Gravina, G. L., et al. (2007). 'Uncoupling of the epidermal growth factor receptor from downstream signal transduction molecules guides the acquired resistance to gefitinib in prostate cancer cells.' Oncol Rep 18(2): 503-511. Frew, A. J., Johnstone, R. W., et al. (2009). 'Enhancing the apoptotic and therapeutic effects of HDAC inhibitors.' Cancer Lett 280(2): 125-133. Fukuoka, M., Yano, S., et al. (2003). 'Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer (The IDEAL 1 Trial) [corrected].' J Clin Oncol 21(12): 2237-2246. Galanis, E., Jaeckle, K. A., et al. (2009). 'Phase II trial of vorinostat in recurrent glioblastoma multiforme: a north central cancer treatment group study.' J Clin Oncol 27(12): 2052-2058. Gatzemeier, U., Pluzanska, A., et al. (2007). 'Phase III study of erlotinib in combination with cisplatin and gemcitabine in advanced non-small-cell lung cancer: the Tarceva Lung Cancer Investigation Trial.' J Clin Oncol 25(12): 1545-1552. Gerber, D. E. and Minna, J. D. (2010). 'ALK inhibition for non-small cell lung cancer: from discovery to therapy in record time.' Cancer Cell 18(6): 548-551. Giaccone, G., Herbst, R. S., et al. (2004). 'Gefitinib in combination with gemcitabine and cisplatin in advanced non-small-cell lung cancer: a phase III trial--INTACT 1.' J Clin Oncol 22(5): 777-784. Glaser, K. B. (2007). 'HDAC inhibitors: clinical update and mechanism-based potential.' Biochem Pharmacol 74(5): 659-671. Glozak, M. A., Sengupta, N., et al. (2005). 'Acetylation and deacetylation of non-histone proteins.' Gene 363: 15-23. Gong, Y., Somwar, R., et al. (2007). 'Induction of BIM is essential for apoptosis triggered by EGFR kinase inhibitors in mutant EGFR-dependent lung adenocarcinomas.' PLoS Med 4(10): e294. Gong, Y., Yao, E., et al. (2009). 'High expression levels of total IGF-1R and sensitivity of NSCLC cells in vitro to an anti-IGF-1R antibody (R1507).' PLoS One 4(10): e7273. Gow, C. H., Shih, J. Y., et al. (2005). 'Acquired gefitinib-resistant mutation of EGFR in a chemonaive lung adenocarcinoma harboring gefitinib-sensitive mutation L858R.' PLoS Med 2(9): e269. Greulich, H., Chen, T. H., et al. (2005). 'Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants.' PLoS Med 2(11): e313. Guix, M., Faber, A. C., et al. (2008). 'Acquired resistance to EGFR tyrosine kinase inhibitors in cancer cells is mediated by loss of IGF-binding proteins.' J Clin Invest 118(7): 2609-2619. Haberland, M., Montgomery, R. L., et al. (2009). 'The many roles of histone deacetylases in development and physiology: implications for disease and therapy.' Nat Rev Genet 10(1): 32-42. Harris, T. (2010). 'Does large scale DNA sequencing of patient and tumor DNA yet provide clinically actionable information?' Discov Med 10(51): 144-150. Herbst, R. S., Giaccone, G., et al. (2004). 'Gefitinib in combination with paclitaxel and carboplatin in advanced non-small-cell lung cancer: a phase III trial--INTACT 2.' J Clin Oncol 22(5): 785-794. Herbst, R. S., Heymach, J. V., et al. (2008). 'Lung cancer.' N Engl J Med 359(13): 1367-1380. Herbst, R. S., Maddox, A. M., et al. (2002). 'Selective oral epidermal growth factor receptor tyrosine kinase inhibitor ZD1839 is generally well-tolerated and has activity in non-small-cell lung cancer and other solid tumors: results of a phase I trial.' J Clin Oncol 20(18): 3815-3825. Herbst, R. S., Prager, D., et al. (2005). 'TRIBUTE: a phase III trial of erlotinib hydrochloride (OSI-774) combined with carboplatin and paclitaxel chemotherapy in advanced non-small-cell lung cancer.' J Clin Oncol 23(25): 5892-5899. Hidalgo, M., Siu, L. L., et al. (2001). 'Phase I and pharmacologic study of OSI-774, an epidermal growth factor receptor tyrosine kinase inhibitor, in patients with advanced solid malignancies.' J Clin Oncol 19(13): 3267-3279. Holbro, T., Civenni, G., et al. (2003). 'The ErbB receptors and their role in cancer progression.' Exp Cell Res 284(1): 99-110. Horn, L. and Pao, W. (2009). 'EML4-ALK: honing in on a new target in non-small-cell lung cancer.' J Clin Oncol 27(26): 4232-4235. Huang, W. C., Chen, Y. J., et al. (2011). 'Nuclear Translocation of Epidermal Growth Factor Receptor by Akt-dependent Phosphorylation Enhances Breast Cancer-resistant Protein Expression in Gefitinib-resistant Cells.' J Biol Chem 286(23): 20558-20568. Hubbert, C., Guardiola, A., et al. (2002). 'HDAC6 is a microtubule-associated deacetylase.' Nature 417(6887): 455-458. Hurbin, A., Wislez, M., et al. (2011). 'Insulin-like growth factor-1 receptor inhibition overcomes gefitinib resistance in mucinous lung adenocarcinoma.' J Pathol. Hynes, N. E. and Lane, H. A. (2005). 'ERBB receptors and cancer: the complexity of targeted inhibitors.' Nat Rev Cancer 5(5): 341-354. Imai, K. and Takaoka, A. (2006). 'Comparing antibody and small-molecule therapies for cancer.' Nat Rev Cancer 6(9): 714-727. Inoue, A., Kobayashi, K., et al. (2009). 'First-line gefitinib for patients with advanced non-small-cell lung cancer harboring epidermal growth factor receptor mutations without indication for chemotherapy.' J Clin Oncol 27(9): 1394-1400. Inoue, S., Riley, J., et al. (2007). 'Apoptosis induced by histone deacetylase inhibitors in leukemic cells is mediated by Bim and Noxa.' Leukemia 21(8): 1773-1782. Insinga, A., Monestiroli, S., et al. (2005). 'Inhibitors of histone deacetylases induce tumor-selective apoptosis through activation of the death receptor pathway.' Nat Med 11(1): 71-76. Jackman, D., Pao, W., et al. (2010). 'Clinical definition of acquired resistance to epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer.' J Clin Oncol 28(2): 357-360. Janku, F., Stewart, D. J., et al. (2010). 'Targeted therapy in non-small-cell lung cancer--is it becoming a reality?' Nat Rev Clin Oncol 7(7): 401-414. Janne, P. A., Engelman, J. A., et al. (2005). 'Epidermal growth factor receptor mutations in non-small-cell lung cancer: implications for treatment and tumor biology.' J Clin Oncol 23(14): 3227-3234. Jemal, A., Siegel, R., et al. (2010). 'Cancer statistics, 2010.' CA Cancer J Clin 60(5): 277-300. Jiang, K., Sun, J., et al. (2004). 'Akt mediates Ras downregulation of RhoB, a suppressor of transformation, invasion, and metastasis.' Mol Cell Biol 24(12): 5565-5576. Jorissen, R. N., Walker, F., et al. (2003). 'Epidermal growth factor receptor: mechanisms of activation and signalling.' Exp Cell Res 284(1): 31-53. Joseph, J., Mudduluru, G., et al. (2004). 'Expression profiling of sodium butyrate (NaB)-treated cells: identification of regulation of genes related to cytokine signaling and cancer metastasis by NaB.' Oncogene 23(37): 6304-6315. Juan, L. J., Shia, W. J., et al. (2000). 'Histone deacetylases specifically down-regulate p53-dependent gene activation.' J Biol Chem 275(27): 20436-20443. Kang, J. H., Kim, M. J., et al. (2008). 'CCAAT box is required for the induction of human thrombospondin-1 gene by trichostatin A.' J Cell Biochem 104(4): 1192-1203. Kawano, O., Sasaki, H., et al. (2006). 'PIK3CA mutation status in Japanese lung cancer patients.' Lung Cancer 54(2): 209-215. Kim, M. S., Kwon, H. J., et al. (2001). 'Histone deacetylases induce angiogenesis by negative regulation of tumor suppressor genes.' Nat Med 7(4): 437-443. Kobayashi, S., Boggon, T. J., et al. (2005). 'EGFR mutation and resistance of non-small-cell lung cancer to gefitinib.' N Engl J Med 352(8): 786-792. Kris, M. G., Natale, R. B., et al. (2003). 'Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial.' JAMA 290(16): 2149-2158. Kumar, A., Petri, E. T., et al. (2008). 'Structure and clinical relevance of the epidermal growth factor receptor in human cancer.' J Clin Oncol 26(10): 1742-1751. Kurai, J., Chikumi, H., et al. (2007). 'Antibody-dependent cellular cytotoxicity mediated by cetuximab against lung cancer cell lines.' Clin Cancer Res 13(5): 1552-1561. Kurtze, I., Sonnemann, J., et al. (2011). 'KRAS-mutated non-small cell lung cancer cells are responsive to either co-treatment with erlotinib or gefitinib and histone deacetylase inhibitors or single treatment with lapatinib.' Oncol Rep 25(4): 1021-1029. Kwak, E. L., Sordella, R., et al. (2005). 'Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib.' Proc Natl Acad Sci U S A 102(21): 7665-7670. Ladanyi, M. and Pao, W. (2008). 'Lung adenocarcinoma: guiding EGFR-targeted therapy and beyond.' Mod Pathol 21 Suppl 2: S16-22. Lafon-Hughes, L., Di Tomaso, M. V., et al. (2008). 'Chromatin-remodelling mechanisms in cancer.' Mutat Res 658(3): 191-214. Le Calvez, F., Mukeria, A., et al. (2005). 'TP53 and KRAS mutation load and types in lung cancers in relation to tobacco smoke: distinct patterns in never, former, and current smokers.' Cancer Res 65(12): 5076-5083. Li, D., Ambrogio, L., et al. (2008). 'BIBW2992, an irreversible EGFR/HER2 inhibitor highly effective in preclinical lung cancer models.' Oncogene 27(34): 4702-4711. Li, D., Shimamura, T., et al. (2007). 'Bronchial and peripheral murine lung carcinomas induced by T790M-L858R mutant EGFR respond to HKI-272 and rapamycin combination therapy.' Cancer Cell 12(1): 81-93. Linardou, H., Dahabreh, I. J., et al. (2009). 'Somatic EGFR mutations and efficacy of tyrosine kinase inhibitors in NSCLC.' Nat Rev Clin Oncol 6(6): 352-366. Linardou, H., Dahabreh, I. J., et al. (2008). 'Assessment of somatic k-RAS mutations as a mechanism associated with resistance to EGFR-targeted agents: a systematic review and meta-analysis of studies in advanced non-small-cell lung cancer and metastatic colorectal cancer.' Lancet Oncol 9(10): 962-972. Liu, B., Fang, M., et al. (2000). 'Induction of apoptosis and activation of the caspase cascade by anti-EGF receptor monoclonal antibodies in DiFi human colon cancer cells do not involve the c-jun N-terminal kinase activity.' Br J Cancer 82(12): 1991-1999. Liu, L. T., Chang, H. C., et al. (2003). 'Histone deacetylase inhibitor up-regulates RECK to inhibit MMP-2 activation and cancer cell invasion.' Cancer Res 63(12): 3069-3072. Loprevite, M., Tiseo, M., et al. (2005). 'In vitro study of CI-994, a histone deacetylase inhibitor, in non-small cell lung cancer cell lines.' Oncol Res 15(1): 39-48. Luger, K., Mader, A. W., et al. (1997). 'Crystal structure of the nucleosome core particle at 2.8 A resolution.' Nature 389(6648): 251-260. Lynch, T. J., Bell, D. W., et al. (2004). 'Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib.' N Engl J Med 350(21): 2129-2139. Lynch, T. J., Patel, T., et al. (2010). 'Cetuximab and first-line taxane/carboplatin chemotherapy in advanced non-small-cell lung cancer: results of the randomized multicenter phase III trial BMS099.' J Clin Oncol 28(6): 911-917. Marks, P. A., Richon, V. M., et al. (2000). 'Histone deacetylase inhibitors: inducers of differentiation or apoptosis of transformed cells.' J Natl Cancer Inst 92(15): 1210-1216. Marks, P., Rifkind, R. A., et al. (2001). 'Histone deacetylases and cancer: causes and therapies.' Nat Rev Cancer 1(3): 194-202. Marone, R., Hess, D., et al. (2004). 'Memo mediates ErbB2-driven cell motility.' Nat Cell Biol 6(6): 515-522. Mayr, N. A., Hussey, D. H., et al. (1995). 'Cost-effectiveness of high-contrast-dose MR screening of asymptomatic brain metastasis.' AJNR Am J Neuroradiol 16(1): 215-217. Michel, F., Soler, M., et al. (1991). 'Initial staging of non-small cell lung cancer: value of routine radioisotope bone scanning.' Thorax 46(7): 469-473. Miller, V. A., Kris, M. G., et al. (2004). 'Bronchioloalveolar pathologic subtype and smoking history predict sensitivity to gefitinib in advanced non-small-cell lung cancer.' J Clin Oncol 22(6): 1103-1109. Minucci, S. and Pelicci, P. G. (2006). 'Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer.' Nat Rev Cancer 6(1): 38-51. Moscatello, D. K., Holgado-Madruga, M., et al. (1995). 'Frequent expression of a mutant epidermal growth factor receptor in multiple human tumors.' Cancer Res 55(23): 5536-5539. Mountain, C. F. (1997). 'Revisions in the International System for Staging Lung Cancer.' Chest 111(6): 1710-1717. Nakagawa, K., Tamura, T., et al. (2003). 'Phase I pharmacokinetic trial of the selective oral epidermal growth factor receptor tyrosine kinase inhibitor gefitinib ('Iressa', ZD1839) in Japanese patients with solid malignant tumors.' Ann Oncol 14(6): 922-930. Network, National Comprehensive Cancer, Ed. (2008). NCCN clinical practice guidelines in oncology: non-small cell lung cancer. Nicholson, R. I., Gee, J. M., et al. (2001). 'EGFR and cancer prognosis.' Eur J Cancer 37 Suppl 4: S9-15. Nimmanapalli, R., Fuino, L., et al. (2003). 'Histone deacetylase inhibitor LAQ824 both lowers expression and promotes proteasomal degradation of Bcr-Abl and induces apoptosis of imatinib mesylate-sensitive or -refractory chronic myelogenous leukemia-blast crisis cells.' Cancer Res 63(16): 5126-5135. Nimmanapalli, R., Fuino, L., et al. (2003). 'Cotreatment with the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) enhances imatinib-induced apoptosis of Bcr-Abl-positive human acute leukemia cells.' Blood 101(8): 3236-3239. Noh, E. J. and Lee, J. S. (2003). 'Functional interplay between modulation of histone deacetylase activity and its regulatory role in G2-M transition.' Biochem Biophys Res Commun 310(2): 267-273. Nyati, M. K., Morgan, M. A., et al. (2006). 'Integration of EGFR inhibitors with radiochemotherapy.' Nat Rev Cancer 6(11): 876-885. Ogiso, H., Ishitani, R., et al. (2002). 'Crystal structure of the complex of human epidermal growth factor and receptor extracellular domains.' Cell 110(6): 775-787. Okamoto, K., Okamoto, I., et al. (2010). 'Role of survivin in EGFR inhibitor-induced apoptosis in non-small cell lung cancers positive for EGFR mutations.' Cancer Res 70(24): 10402-10410. Okawara, G., Ung, Y. C., et al. (2004). 'Postoperative radiotherapy in stage II or IIIA completely resected non-small cell lung cancer: a systematic review and practice guideline.' Lung Cancer 44(1): 1-11. Ozaki, K., Kosugi, M., et al. (2010). 'Blockade of the ERK or PI3K-Akt signaling pathway enhances the cytotoxicity of histone deacetylase inhibitors in tumor cells resistant to gefitinib or imatinib.' Biochem Biophys Res Commun 391(4): 1610-1615. P. A. Janne, J. H. Schellens, J. A. Engelman, S. G. Eckhardt, R. Millham, L. J. Denis, C. D. Britten, S. G. Wong, D. S. Boss, D. R. Camidge (2008). Preliminary activity and safety results from a phase I clinical trial of PF-00299804, an irreversible pan-HER inhibitor, in patients (pts) with NSCLC J Clin Oncol (Meeting Abstracts). 26 Paez, J. G., Janne, P. A., et al. (2004). 'EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy.' Science 304(5676): 1497-1500. Pao, W. and Chmielecki, J. (2010). 'Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer.' Nat Rev Cancer 10(11): 760-774. Pao, W. and Girard, N. (2011). 'New driver mutations in non-small-cell lung cancer.' Lancet Oncol 12(2): 175-180. Pao, W., Kris, M. G., et al. (2009). 'Integration of molecular profiling into the lung cancer clinic.' Clin Cancer Res 15(17): 5317-5322. Pao, W. and Miller, V. A. (2005). 'Epidermal growth factor receptor mutations, small-molecule kinase inhibitors, and non-small-cell lung cancer: current knowledge and future directions.' J Clin Oncol 23(11): 2556-2568. Pao, W., Miller, V. A., et al. (2005). 'Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain.' PLoS Med 2(3): e73. Pao, W., Miller, V., et al. (2004). 'EGF receptor gene mutations are common in lung cancers from 'never smokers' and are associated with sensitivity of tumors to gefitinib and erlotinib.' Proc Natl Acad Sci U S A 101(36): 13306-13311. Parthun, M. R. (2007). 'Hat1: the emerging cellular roles of a type B histone acetyltransferase.' Oncogene 26(37): 5319-5328. Pauer, L. R., Olivares, J., et al. (2004). 'Phase I study of oral CI-994 in combination with carboplatin and paclitaxel in the treatment of patients with advanced solid tumors.' Cancer Invest 22(6): 886-896. Pearson, F. G. (1999). 'Non-small cell lung cancer: role of surgery for stages I-III.' Chest 116(6 Suppl): 500S-503S. Perez-Soler, R., Chachoua, A., et al. (2004). 'Determinants of tumor response and survival with erlotinib in patients with non--small-cell lung cancer.' J Clin Oncol 22(16): 3238-3247. Pirker, R., Pereira, J. R., et al. (2009). 'Cetuximab plus chemotherapy in patients with advanced non-small-cell lung cancer (FLEX): an open-label randomised phase III trial.' Lancet 373(9674): 1525-1531. Politi, K., Fan, P. D., et al. (2010). 'Erlotinib resistance in mouse models of epidermal growth factor receptor-induced lung adenocarcinoma.' Dis Model Mech 3(1-2): 111-119. Prewett, M., Rockwell, P., et al. (1996). 'The biologic effects of C225, a chimeric monoclonal antibody to the EGFR, on human prostate carcinoma.' J Immunother Emphasis Tumor Immunol 19(6): 419-427. Qian, D. Z., Kato, Y., et al. (2006). 'Targeting tumor angiogenesis with histone deacetylase inhibitors: the hydroxamic acid derivative LBH589.' Clin Cancer Res 12(2): 634-642. Rahmani, M., Yu, C., et al. (2003). 'Inhibition of PI-3 kinase sensitizes human leukemic cells to histone deacetylase inhibitor-mediated apoptosis through p44/42 MAP kinase inactivation and abrogation of p21(CIP1/WAF1) induction rather than AKT inhibition.' Oncogene 22(40): 6231-6242. Ranson, M., Hammond, L. A., et al. (2002). 'ZD1839, a selective oral epidermal growth factor receptor-tyrosine kinase inhibitor, is well tolerated and active in patients with solid, malignant tumors: results of a phase I trial.' J Clin Oncol 20(9): 2240-2250. Rosato, R. R., Almenara, J. A., et al. (2004). 'Evidence of a functional role for p21WAF1/CIP1 down-regulation in synergistic antileukemic interactions between the histone deacetylase inhibitor sodium butyrate and flavopiridol.' Mol Pharmacol 65(3): 571-581. Rosato, R. R., Maggio, S. C., et al. (2006). 'The histone deacetylase inhibitor LAQ824 induces human leukemia cell death through a process involving XIAP down-regulation, oxidative injury, and the acid sphingomyelinase-dependent generation of ceramide.' Mol Pharmacol 69(1): 216-225. Rosell, R., Moran, T., et al. (2009). 'Screening for epidermal growth factor receptor mutations in lung cancer.' N Engl J Med 361(10): 958-967. Salomon, D. S., Brandt, R., et al. (1995). 'Epidermal growth factor-related peptides and their receptors in human malignancies.' Crit Rev Oncol Hematol 19(3): 183-232. Sasaki, T., Rodig, S. J., et al. (2010). 'The biology and treatment of EML4-ALK non-small cell lung cancer.' Eur J Cancer 46(10): 1773-1780. Scagliotti, G. V., Parikh, P., et al. (2008). 'Phase III study comparing cisplatin plus gemcitabine with cisplatin plus pemetrexed in chemotherapy-naive patients with advanced-stage non-small-cell lung cancer.' J Clin Oncol 26(21): 3543-3551. Sharma, S. V., Lee, D. Y., et al. (2010). 'A chromatin-mediated reversible drug-tolerant state in cancer cell subpopulations.' Cell 141(1): 69-80. Shaw, A. T., Yeap, B. Y., et al. (2009). 'Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK.' J Clin Oncol 27(26): 4247-4253. Shawver, L. K., Slamon, D., et al. (2002). 'Smart drugs: tyrosine kinase inhibitors in cancer therapy.' Cancer Cell 1(2): 117-123. Shepherd, F. A., Rodrigues Pereira, J., et al. (2005). 'Erlotinib in previously treated non-small-cell lung cancer.' N Engl J Med 353(2): 123-132. Shigematsu, H., Lin, L., et al. (2005). 'Clinical and biological features associated with epidermal growth factor receptor gene mutations in lung cancers.' J Natl Cancer Inst 97(5): 339-346. Shih, J. Y., Gow, C. H., et al. (2005). 'EGFR mutation conferring primary resistance to gefitinib in non-small-cell lung cancer.' N Engl J Med 353(2): 207-208. Shtiegman, K. and Yarden, Y. (2003). 'The role of ubiquitylation in signaling by growth factors: implications to cancer.' Semin Cancer Biol 13(1): 29-40. Sibilia, M., Kroismayr, R., et al. (2007). 'The epidermal growth factor receptor: from development to tumorigenesis.' Differentiation 75(9): 770-787. Sjogren, S., Inganas, M., et al. (1998). 'Prognostic and predictive value of c-erbB-2 overexpression in primary breast cancer, alone and in combination with other prognostic markers.' J Clin Oncol 16(2): 462-469. Soda, M., Choi, Y. L., et al. (2007). 'Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer.' Nature 448(7153): 561-566. Solit, D. B., Garraway, L. A., et al. (2006). 'BRAF mutation predicts sensitivity to MEK inhibition.' Nature 439(7074): 358-362. Sos, M. L., Koker, M., et al. (2009). 'PTEN loss contributes to erlotinib resistance in EGFR-mutant lung cancer by activation of Akt and EGFR.' Cancer Res 69(8): 3256-3261. Spira, A. and Ettinger, D. S. (2004). 'Multidisciplinary management of lung cancer.' N Engl J Med 350(4): 379-392. Sun, S., Schiller, J. H., et al. (2007). 'Lung cancer in never smokers--a different disease.' Nat Rev Cancer 7(10): 778-790. Sunpaweravong, P., Sunpaweravong, S., et al. (2005). 'Epidermal growth factor receptor and cyclin D1 are independently amplified and overexpressed in esophageal squamous cell carcinoma.' J Cancer Res Clin Oncol 131(2): 111-119. T. J. Lynch, R. Lilenbaum, P. Bonomi, R. Ansari, R. Govindan, P. A. Janne, N. Hanna (2004). 'A phase II trial of cetuximab as therapy for recurrent non-small cell lung cancer (NSCLC). (abstract no. 7084).' J Clin Oncol. Tahara, R. W., Lackner, R. P., et al. (2000). 'Is there a role for routine mediastinoscopy in patients with peripheral T1 lung cancers?' Am J Surg 180(6): 488-491; discussion 491-482. Tam, I. Y., Chung, L. P., et al. (2006). 'Distinct epidermal growth factor receptor and KRAS mutation patterns in non-small cell lung cancer patients with different tobacco exposure and clinicopathologic features.' Clin Cancer Res 12(5): 1647-1653. Tam, I. Y., Leung, E. L., et al. (2009). 'Double EGFR mutants containing rare EGFR mutant types show reduced in vitro response to gefitinib compared with common activating missense mutations.' Mol Cancer Ther 8(8): 2142-2151. Turke, A. B., Zejnullahu, K., et al. (2010). 'Preexistence and clonal selection of MET amplification in EGFR mutant NSCLC.' Cancer Cell 17(1): 77-88. van Zandwijk, N., Mathy, A., et al. (2007). 'EGFR and KRAS mutations as criteria for treatment with tyrosine kinase inhibitors: retro- and prospective observations in non-small-cell lung cancer.' Ann Oncol 18(1): 99-103. Vivanco, I., Rohle, D., et al. (2010). 'The phosphatase and tensin homolog regulates epidermal growth factor receptor (EGFR) inhibitor response by targeting EGFR for degradation.' Proc Natl Acad Sci U S A 107(14): 6459-6464. Wang, G. G., Allis, C. D., et al. (2007). 'Chromatin remodeling and cancer, Part I: Covalent histone modifications.' Trends Mol Med 13(9): 363-372. Weir, B. A., Woo, M. S., et al. (2007). 'Characterizing the cancer genome in lung adenocarcinoma.' Nature 450(7171): 893-898. Weisenburger, T. H. (1994). 'Effects of postoperative mediastinal radiation on completely resected stage II and stage III epidermoid cancer of the lung. LCSG 773.' Chest 106(6 Suppl): 297S-301S. Weng, E., Tran, L., et al. (2000). 'Accuracy and clinical impact of mediastinal lymph node staging with FDG-PET imaging in potentially resectable lung cancer.' Am J Clin Oncol 23(1): 47-52. Wheeler, D. L., Dunn, E. F., et al. (2010). 'Understanding resistance to EGFR inhibitors-impact on future treatment strategies.' Nat Rev Clin Oncol 7(9): 493-507. Witta, S. E., Dziadziuszko, R., et al. (2009). 'ErbB-3 expression is associated with E-cadherin and their coexpression restores response to gefitinib in non-smal | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/29252 | - |
dc.description.abstract | 非小細胞肺癌(NSCLC) 會表現過度活化之epidermal growth factor receptor (EGFR),促進腫瘤形成。EGFR-tyrosine kinase inhibitors (EGFR-TKIs) 如gefitinib與erlotinib,能抑制過度活化之EGFR,使癌細胞無法增生及轉移,用於治療EGFR突變之非小細胞肺癌;然而TKI 治療後如產生EGFR 之T790M 突變或MET 之gene amplification,造成治療失敗,即為secondary resistance,而克服secondary resistance是非小細胞肺癌治療之關鍵問題。
在許多腫瘤中HDAC 有過度表現,而降低抑癌基因之表現,因此HDAC 為癌症治療之熱門標的,HDAC 抑制劑可經由調節染色質組蛋白及non-histone protein之乙醯化,誘發癌細胞死亡、凋亡及細胞週期停滯而有抗癌效果。 本實驗篩選出HDAC 抑制劑compound D,可抑制NSCLC 之細胞生長及減少EGFR 與MET 之表現。Compound D 與gefitinib 合併使用,對gefitinib 具抗藥性細胞之生長有加成性抑制作用,亦抑制其下游AKT 及ERK 之活化,並促進癌細胞凋亡。在動物模式中,併用compound D 與gefitinib 可顯著抑制腫瘤生長。因此,gefitinib 併用HDAC 抑制劑可克服gefitinib 之抗藥性,對於產生secondary resistance之NSCLC 病患是具潛力之治療策略。 | zh_TW |
dc.description.abstract | Epidermal growth factor receptor (EGFR), a receptor tyrosine kinase, which plays a pivotal role in cancer progression, is aberrantly overexpressed and abnormally
activated in many cancers, such as non-small-cell lung cancer (NSCLC). EGFR-tyrosine kinase inhibitors (EGFR-TKIs) gefitinib and erlotinib have been shown to improve overall survival and approved for the treatment of EGFR-mutant NSCLC. Recently, it has been signified that primary and secondary resistance to EGFR-TKIs limits their clinical significance. For instance, T790M mutation in EGFR or c-MET gene amplification makes up most cases of secondary resistance. Targeting mutant EGFR or c-MET could overcome TKI resistance in NSCLC. In our study, combination of gefitinib with HDAC inhibitor compound D overcomes TKI resistance in NSCLC cell lines. Compound D down-regulated EGFR and MET, and then disturbed the phosphorylation of AKT and ERK in NSCLC. Combination of compound D and gefitinib showed a synergistic antiproliferative effect through decreasing the activities of AKT and ERK and increasing apoptotic cell death. In addition, the compound D/gefitinib combination potentially inhibited in vivo tumor growth. Our data suggest that the compound D/gefitinib combination represents a promising strategy to overcome EGFR-TKI resistance in NSCLC. | en |
dc.description.provenance | Made available in DSpace on 2021-06-13T01:03:24Z (GMT). No. of bitstreams: 1 ntu-100-R98443012-1.pdf: 6903138 bytes, checksum: 15209ea26ad0f045e8818246f509e4b7 (MD5) Previous issue date: 2011 | en |
dc.description.tableofcontents | 縮寫表................................................ i
中文摘要.............................................. v Abstract.............................................. vi 第一章 緒論........................................... 1 第一節 非小細胞肺癌................................... 2 非小細胞肺癌之腫瘤分期及治療.......................... 2 第二節 非小細胞肺癌中基因之變異....................... 8 EGFR 訊息傳遞......................................... 8 EGFR 突變............................................. 10 其它之基因變異........................................ 11 標靶治療.............................................. 11 第三節 對小分子藥物之抗藥性........................... 24 原發抗藥性............................................ 24 繼發抗藥性............................................ 25 克服TKI 之抗藥性...................................... 26 第四節 HDAC 抑制劑於癌症之應用........................ 35 組蛋白之乙醯化及去乙醯化.............................. 36 HDAC 抑制劑........................................... 37 研究動機.............................................. 47 第二章 實驗材料與方法................................. 48 第三章 實驗結果....................................... 54 第四章 討論........................................... 85 參考資料.............................................. 91 | |
dc.language.iso | zh-TW | |
dc.title | HDAC抑制劑克服非小細胞肺癌之 gefitinib抗藥性之研究 | zh_TW |
dc.title | HDAC inhibitor overcomes the gefitinib resistance in non-small-cell lung cancer | en |
dc.type | Thesis | |
dc.date.schoolyear | 99-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 吳明賢,黃偉謙 | |
dc.subject.keyword | 非小細胞肺癌,HDAC抑制劑,Gefitinib, | zh_TW |
dc.subject.keyword | NSCLC,HDAC inhibitor,Gefitinib, | en |
dc.relation.page | 104 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2011-08-04 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 藥理學研究所 | zh_TW |
顯示於系所單位: | 藥理學科所 |
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