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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 郭彥彬(Mark Yen-Ping Kuo) | |
dc.contributor.author | Tsung-Han Hsieh | en |
dc.contributor.author | 謝宗翰 | zh_TW |
dc.date.accessioned | 2021-06-15T02:49:25Z | - |
dc.date.available | 2014-09-15 | |
dc.date.copyright | 2009-09-15 | |
dc.date.issued | 2009 | |
dc.date.submitted | 2009-08-05 | |
dc.identifier.citation | 1. Vokes EE, Weichselbaum RR, Lippman SM, Hong WK. Head and neck cancer. N Engl J Med 1993;328:184-94.
2. Haddad RI, Shin DM. Recent advances in head and neck cancer. N Engl J Med 2008;359:1143-54. 3. Forastiere A, Koch W, Trotti A, Sidransky D. Head and neck cancer. N Engl J Med 2001;345:1890-900. 4. Liao CT, Chang JT, Wang HM, et al. Analysis of risk factors of predictive local tumor control in oral cavity cancer. Ann Surg Oncol 2008;15:915-22. 5. Liao CT, Kang CJ, Chang JT, et al. Survival of second and multiple primary tumors in patients with oral cavity squamous cell carcinoma in the betel quid chewing area. Oral Oncol 2007;43:811-9. 6. Ko YC, Huang YL, Lee CH, Chen MJ, Lin LM, Tsai CC. Betel quid chewing, cigarette smoking and alcohol consumption related to oral cancer in Taiwan. J Oral Pathol Med 1995;24:450-3. 7. Koch WM, Lango M, Sewell D, Zahurak M, Sidransky D. Head and neck cancer in nonsmokers: a distinct clinical and molecular entity. Laryngoscope 1999;109:1544-51. 8. Sankaranarayanan R, Duffy SW, Padmakumary G, Day NE, Krishan Nair M. Risk factors for cancer of the buccal and labial mucosa in Kerala, southern India. J Epidemiol Community Health 1990;44:286-92. 9. Sankaranarayanan R, Duffy SW, Padmakumary G, Day NE, Padmanabhan TK. Tobacco chewing, alcohol and nasal snuff in cancer of the gingiva in Kerala, India. Br J Cancer 1989;60:638-43. 10. Yang YH, Chen CH, Chang JS, Lin CC, Cheng TC, Shieh TY. Incidence rates of oral cancer and oral pre-cancerous lesions in a 6-year follow-up study of a Taiwanese aboriginal community. J Oral Pathol Med 2005;34:596-601. 11. Yang YH, Lee HY, Tung S, Shieh TY. Epidemiological survey of oral submucous fibrosis and leukoplakia in aborigines of Taiwan. J Oral Pathol Med 2001;30:213-9. 12. Lai KC, Lee TC. Genetic damage in cultured human keratinocytes stressed by long-term exposure to areca nut extracts. Mutat Res 2006;599:66-75. 13. Sundqvist K, Liu Y, Nair J, Bartsch H, Arvidson K, Grafstrom RC. Cytotoxic and genotoxic effects of areca nut-related compounds in cultured human buccal epithelial cells. Cancer Res 1989;49:5294-8. 14. Dave BJ, Trivedi AH, Adhvaryu SG. Role of areca nut consumption in the cause of oral cancers. A cytogenetic assessment. Cancer 1992;70:1017-23. 15. Jeng JH, Chang MC, Hahn LJ. Role of areca nut in betel quid-associated chemical carcinogenesis: current awareness and future perspectives. Oral Oncol 2001;37:477-92. 16. Lee PH, Chang MC, Chang WH, et al. Prolonged exposure to arecoline arrested human KB epithelial cell growth: regulatory mechanisms of cell cycle and apoptosis. Toxicology 2006;220:81-9. 17. Mashberg A. Erythroplasia vs. leukoplasia in the diagnosis of early asymptomatic oral squamous carcinoma. N Engl J Med 1977;297:109-10. 18. Shklar GS. Oral leukoplakia. N Engl J Med 1986;315:1544-6. 19. Dassonville O, Formento JL, Francoual M, et al. Expression of epidermal growth factor receptor and survival in upper aerodigestive tract cancer. J Clin Oncol 1993;11:1873-8. 20. Mendelsohn J, Fan Z. Epidermal growth factor receptor family and chemosensitization. J Natl Cancer Inst 1997;89:341-3. 21. Rubin Grandis J, Melhem MF, Gooding WE, et al. Levels of TGF-alpha and EGFR protein in head and neck squamous cell carcinoma and patient survival. J Natl Cancer Inst 1998;90:824-32. 22. Patel V, Senderowicz AM, Pinto D, Jr., et al. Flavopiridol, a novel cyclin-dependent kinase inhibitor, suppresses the growth of head and neck squamous cell carcinomas by inducing apoptosis. J Clin Invest 1998;102:1674-81. 23. Hashemolhosseini S, Nagamine Y, Morley SJ, Desrivieres S, Mercep L, Ferrari S. Rapamycin inhibition of the G1 to S transition is mediated by effects on cyclin D1 mRNA and protein stability. J Biol Chem 1998;273:14424-9. 24. Shah JP. Patterns of cervical lymph node metastasis from squamous carcinomas of the upper aerodigestive tract. Am J Surg 1990;160:405-9. 25. Chiang AC, Massague J. Molecular basis of metastasis. N Engl J Med 2008;359:2814-23. 26. Gupta GP, Massague J. Cancer metastasis: building a framework. Cell 2006;127:679-95. 27. Nguyen DX, Bos PD, Massague J. Metastasis: from dissemination to organ-specific colonization. Nat Rev Cancer 2009;9:274-84. 28. Fidler IJ. The pathogenesis of cancer metastasis: the 'seed and soil' hypothesis revisited. Nat Rev Cancer 2003;3:453-8. 29. Choi HR, Sturgis EM, Rosenthal DI, Luna MA, Batsakis JG, El-Naggar AK. Sarcomatoid carcinoma of the head and neck: molecular evidence for evolution and progression from conventional squamous cell carcinomas. Am J Surg Pathol 2003;27:1216-20. 30. Janot F, Klijanienko J, Russo A, et al. Prognostic value of clinicopathological parameters in head and neck squamous cell carcinoma: a prospective analysis. Br J Cancer 1996;73:531-8. 31. Diwakar N, Sperandio M, Sherriff M, Brown A, Odell EW. Heterogeneity, histological features and DNA ploidy in oral carcinoma by image-based analysis. Oral Oncol 2005;41:416-22. 32. Wang X, Fan M, Chen X, et al. Intratumor genomic heterogeneity correlates with histological grade of advanced oral squamous cell carcinoma. Oral Oncol 2006;42:740-4. 33. Braakhuis BJ, Tabor MP, Kummer JA, Leemans CR, Brakenhoff RH. A genetic explanation of Slaughter's concept of field cancerization: evidence and clinical implications. Cancer Res 2003;63:1727-30. 34. Jin C, Jin Y, Wennerberg J, Akervall J, Dictor M, Mertens F. Karyotypic heterogeneity and clonal evolution in squamous cell carcinomas of the head and neck. Cancer Genet Cytogenet 2002;132:85-96. 35. Copper MP, Jovanovic A, Nauta JJ, et al. Role of genetic factors in the etiology of squamous cell carcinoma of the head and neck. Arch Otolaryngol Head Neck Surg 1995;121:157-60. 36. Jin YT, Myers J, Tsai ST, Goepfert H, Batsakis JG, el-Naggar AK. Genetic alterations in oral squamous cell carcinoma of young adults. Oral Oncol 1999;35:251-6. 37. el-Naggar AK, Hurr K, Luna MA, Goepfert H, Hong WK, Batsakis JG. Intratumoral genetic heterogeneity in primary head and neck squamous carcinoma using microsatellite markers. Diagn Mol Pathol 1997;6:305-8. 38. El-Naggar AK, Hurr K, Huff V, Clayman GL, Luna MA, Batsakis JG. Microsatellite instability in preinvasive and invasive head and neck squamous carcinoma. Am J Pathol 1996;148:2067-72. 39. Bartolozzi C, Lencioni R. Ethanol injection for the treatment of hepatic tumours. Eur Radiol 1996;6:682-96. 40. Li G, Sturgis EM, Wang LE, et al. Association of a p73 exon 2 G4C14-to-A4T14 polymorphism with risk of squamous cell carcinoma of the head and neck. Carcinogenesis 2004;25:1911-6. 41. El-Naggar AK, Hurr K, Huff V, Luna MA, Goepfert H, Batsakis JG. Allelic loss and replication errors at microsatellite loci on chromosome 11p in head and neck squamous carcinoma: association with aggressive biological features. Clin Cancer Res 1996;2:903-7. 42. Weber A, Wittekind C, Tannapfel A. Genetic and epigenetic alterations of 9p21 gene products in benign and malignant tumors of the head and neck. Pathol Res Pract 2003;199:391-7. 43. Papadimitrakopoulou VA, Izzo J, Mao L, et al. Cyclin D1 and p16 alterations in advanced premalignant lesions of the upper aerodigestive tract: role in response to chemoprevention and cancer development. Clin Cancer Res 2001;7:3127-34. 44. Callender T, el-Naggar AK, Lee MS, Frankenthaler R, Luna MA, Batsakis JG. PRAD-1 (CCND1)/cyclin D1 oncogene amplification in primary head and neck squamous cell carcinoma. Cancer 1994;74:152-8. 45. Gasco M, Crook T. The p53 network in head and neck cancer. Oral Oncol 2003;39:222-31. 46. Boyle JO, Hakim J, Koch W, et al. The incidence of p53 mutations increases with progression of head and neck cancer. Cancer Res 1993;53:4477-80. 47. Hartwell LH, Kastan MB. Cell cycle control and cancer. Science 1994;266:1821-8. 48. Koch WM, Brennan JA, Zahurak M, et al. p53 mutation and locoregional treatment failure in head and neck squamous cell carcinoma. J Natl Cancer Inst 1996;88:1580-6. 49. Berenson JR, Yang J, Mickel RA. Frequent amplification of the bcl-1 locus in head and neck squamous cell carcinomas. Oncogene 1989;4:1111-6. 50. Jares P, Fernandez PL, Campo E, et al. PRAD-1/cyclin D1 gene amplification correlates with messenger RNA overexpression and tumor progression in human laryngeal carcinomas. Cancer Res 1994;54:4813-7. 51. Hanahan D, Weinberg RA. The hallmarks of cancer. Cell 2000;100:57-70. 52. Staller P, Sulitkova J, Lisztwan J, Moch H, Oakeley EJ, Krek W. Chemokine receptor CXCR4 downregulated by von Hippel-Lindau tumour suppressor pVHL. Nature 2003;425:307-11. 53. Higgins DF, Kimura K, Bernhardt WM, et al. Hypoxia promotes fibrogenesis in vivo via HIF-1 stimulation of epithelial-to-mesenchymal transition. J Clin Invest 2007;117:3810-20. 54. Erler JT, Bennewith KL, Nicolau M, et al. Lysyl oxidase is essential for hypoxia-induced metastasis. Nature 2006;440:1222-6. 55. Pardal R, Clarke MF, Morrison SJ. Applying the principles of stem-cell biology to cancer. Nat Rev Cancer 2003;3:895-902. 56. Bonnet D, Dick JE. Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med 1997;3:730-7. 57. Al-Hajj M, Wicha MS, Benito-Hernandez A, Morrison SJ, Clarke MF. Prospective identification of tumorigenic breast cancer cells. Proc Natl Acad Sci U S A 2003;100:3983-8. 58. Singh SK, Hawkins C, Clarke ID, et al. Identification of human brain tumour initiating cells. Nature 2004;432:396-401. 59. Valk-Lingbeek ME, Bruggeman SW, van Lohuizen M. Stem cells and cancer; the polycomb connection. Cell 2004;118:409-18. 60. Beachy PA, Karhadkar SS, Berman DM. Tissue repair and stem cell renewal in carcinogenesis. Nature 2004;432:324-31. 61. Radtke F, Clevers H. Self-renewal and cancer of the gut: two sides of a coin. Science 2005;307:1904-9. 62. Cavallaro U, Christofori G. Cell adhesion and signalling by cadherins and Ig-CAMs in cancer. Nat Rev Cancer 2004;4:118-32. 63. Perl AK, Wilgenbus P, Dahl U, Semb H, Christofori G. A causal role for E-cadherin in the transition from adenoma to carcinoma. Nature 1998;392:190-3. 64. Thiery JP. Epithelial-mesenchymal transitions in tumour progression. Nat Rev Cancer 2002;2:442-54. 65. Yang MH, Wu MZ, Chiou SH, et al. Direct regulation of TWIST by HIF-1alpha promotes metastasis. Nat Cell Biol 2008;10:295-305. 66. Guo W, Giancotti FG. Integrin signalling during tumour progression. Nat Rev Mol Cell Biol 2004;5:816-26. 67. Felding-Habermann B, O'Toole TE, Smith JW, et al. Integrin activation controls metastasis in human breast cancer. Proc Natl Acad Sci U S A 2001;98:1853-8. 68. Wang H, Fu W, Im JH, et al. Tumor cell alpha3beta1 integrin and vascular laminin-5 mediate pulmonary arrest and metastasis. J Cell Biol 2004;164:935-41. 69. Friedl P, Wolf K. Tumour-cell invasion and migration: diversity and escape mechanisms. Nat Rev Cancer 2003;3:362-74. 70. Liotta LA, Kohn EC. The microenvironment of the tumour-host interface. Nature 2001;411:375-9. 71. Clark EA, Golub TR, Lander ES, Hynes RO. Genomic analysis of metastasis reveals an essential role for RhoC. Nature 2000;406:532-5. 72. Kim M, Gans JD, Nogueira C, et al. Comparative oncogenomics identifies NEDD9 as a melanoma metastasis gene. Cell 2006;125:1269-81. 73. Mehlen P, Puisieux A. Metastasis: a question of life or death. Nat Rev Cancer 2006;6:449-58. 74. Stupack DG, Teitz T, Potter MD, et al. Potentiation of neuroblastoma metastasis by loss of caspase-8. Nature 2006;439:95-9. 75. Egeblad M, Werb Z. New functions for the matrix metalloproteinases in cancer progression. Nat Rev Cancer 2002;2:161-74. 76. Condeelis J, Pollard JW. Macrophages: obligate partners for tumor cell migration, invasion, and metastasis. Cell 2006;124:263-6. 77. de Visser KE, Eichten A, Coussens LM. Paradoxical roles of the immune system during cancer development. Nat Rev Cancer 2006;6:24-37. 78. Kalluri R, Zeisberg M. Fibroblasts in cancer. Nat Rev Cancer 2006;6:392-401. 79. Allinen M, Beroukhim R, Cai L, et al. Molecular characterization of the tumor microenvironment in breast cancer. Cancer Cell 2004;6:17-32. 80. Orimo A, Gupta PB, Sgroi DC, et al. Stromal fibroblasts present in invasive human breast carcinomas promote tumor growth and angiogenesis through elevated SDF-1/CXCL12 secretion. Cell 2005;121:335-48. 81. Hanahan D, Folkman J. Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis. Cell 1996;86:353-64. 82. Alitalo K, Tammela T, Petrova TV. Lymphangiogenesis in development and human disease. Nature 2005;438:946-53. 83. Yang J, Mani SA, Donaher JL, et al. Twist, a master regulator of morphogenesis, plays an essential role in tumor metastasis. Cell 2004;117:927-39. 84. Ruiter DJ, van Krieken JH, van Muijen GN, de Waal RM. Tumour metastasis: is tissue an issue? Lancet Oncol 2001;2:109-12. 85. Weis SM, Cheresh DA. Pathophysiological consequences of VEGF-induced vascular permeability. Nature 2005;437:497-504. 86. Criscuoli ML, Nguyen M, Eliceiri BP. Tumor metastasis but not tumor growth is dependent on Src-mediated vascular permeability. Blood 2005;105:1508-14. 87. Padua D, Zhang XH, Wang Q, et al. TGFbeta primes breast tumors for lung metastasis seeding through angiopoietin-like 4. Cell 2008;133:66-77. 88. Roepman P, Wessels LF, Kettelarij N, et al. An expression profile for diagnosis of lymph node metastases from primary head and neck squamous cell carcinomas. Nat Genet 2005;37:182-6. 89. Chung CH, Parker JS, Karaca G, et al. Molecular classification of head and neck squamous cell carcinomas using patterns of gene expression. Cancer Cell 2004;5:489-500. 90. O'Donnell RK, Kupferman M, Wei SJ, et al. Gene expression signature predicts lymphatic metastasis in squamous cell carcinoma of the oral cavity. Oncogene 2005;24:1244-51. 91. Katayama A, Bandoh N, Kishibe K, et al. Expressions of matrix metalloproteinases in early-stage oral squamous cell carcinoma as predictive indicators for tumor metastases and prognosis. Clin Cancer Res 2004;10:634-40. 92. Thompson EW, Newgreen DF, Tarin D. Carcinoma invasion and metastasis: a role for epithelial-mesenchymal transition? Cancer Res 2005;65:5991-5; discussion 5. 93. Thomas GT, Lewis MP, Speight PM. Matrix metalloproteinases and oral cancer. Oral Oncol 1999;35:227-33. 94. de Vicente JC, Fresno MF, Villalain L, Vega JA, Hernandez Vallejo G. Expression and clinical significance of matrix metalloproteinase-2 and matrix metalloproteinase-9 in oral squamous cell carcinoma. Oral Oncol 2005;41:283-93. 95. Patel BP, Shah PM, Rawal UM, et al. Activation of MMP-2 and MMP-9 in patients with oral squamous cell carcinoma. J Surg Oncol 2005;90:81-8. 96. Peled A, Petit I, Kollet O, et al. Dependence of human stem cell engraftment and repopulation of NOD/SCID mice on CXCR4. Science 1999;283:845-8. 97. Guleng B, Tateishi K, Ohta M, et al. Blockade of the stromal cell-derived factor-1/CXCR4 axis attenuates in vivo tumor growth by inhibiting angiogenesis in a vascular endothelial growth factor-independent manner. Cancer Res 2005;65:5864-71. 98. Uchida D, Begum NM, Almofti A, et al. Possible role of stromal-cell-derived factor-1/CXCR4 signaling on lymph node metastasis of oral squamous cell carcinoma. Exp Cell Res 2003;290:289-302. 99. Kerbel R, Folkman J. Clinical translation of angiogenesis inhibitors. Nat Rev Cancer 2002;2:727-39. 100. Carmeliet P, Jain RK. Angiogenesis in cancer and other diseases. Nature 2000;407:249-57. 101. Bergers G, Song S, Meyer-Morse N, Bergsland E, Hanahan D. Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors. J Clin Invest 2003;111:1287-95. 102. Laird AD, Vajkoczy P, Shawver LK, et al. SU6668 is a potent antiangiogenic and antitumor agent that induces regression of established tumors. Cancer Res 2000;60:4152-60. 103. Li M, Ye C, Feng C, et al. Enhanced antiangiogenic therapy of squamous cell carcinoma by combined endostatin and epidermal growth factor receptor-antisense therapy. Clin Cancer Res 2002;8:3570-8. 104. Tseng JE, Glisson BS, Khuri FR, et al. Phase II study of the antiangiogenesis agent thalidomide in recurrent or metastatic squamous cell carcinoma of the head and neck. Cancer 2001;92:2364-73. 105. Vokes EE. Optimal therapy for unresectable stage III non-small-cell lung cancer. J Clin Oncol 2005;23:5853-5. 106. Bruick RK. Oxygen sensing in the hypoxic response pathway: regulation of the hypoxia-inducible transcription factor. Genes Dev 2003;17:2614-23. 107. Iyer NV, Kotch LE, Agani F, et al. Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1 alpha. Genes Dev 1998;12:149-62. 108. Semenza GL. Regulation of mammalian O2 homeostasis by hypoxia-inducible factor 1. Annu Rev Cell Dev Biol 1999;15:551-78. 109. Semenza GL. HIF-1: mediator of physiological and pathophysiological responses to hypoxia. J Appl Physiol 2000;88:1474-80. 110. Semenza GL. HIF-1 and tumor progression: pathophysiology and therapeutics. Trends Mol Med 2002;8:S62-7. 111. Semenza GL. Targeting HIF-1 for cancer therapy. Nat Rev Cancer 2003;3:721-32. 112. Bruick RK, McKnight SL. A conserved family of prolyl-4-hydroxylases that modify HIF. Science 2001;294:1337-40. 113. Epstein AC, Gleadle JM, McNeill LA, et al. C. elegans EGL-9 and mammalian homologs define a family of dioxygenases that regulate HIF by prolyl hydroxylation. Cell 2001;107:43-54. 114. Ivan M, Kondo K, Yang H, et al. HIFalpha targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing. Science 2001;292:464-8. 115. Jaakkola P, Mole DR, Tian YM, et al. Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation. Science 2001;292:468-72. 116. Masson N, Willam C, Maxwell PH, Pugh CW, Ratcliffe PJ. Independent function of two destruction domains in hypoxia-inducible factor-alpha chains activated by prolyl hydroxylation. EMBO J 2001;20:5197-206. 117. Wang GL, Semenza GL. General involvement of hypoxia-inducible factor 1 in transcriptional response to hypoxia. Proc Natl Acad Sci U S A 1993;90:4304-8. 118. Hockel M, Vaupel P. Tumor hypoxia: definitions and current clinical, biologic, and molecular aspects. J Natl Cancer Inst 2001;93:266-76. 119. Hockel M, Schlenger K, Hockel S, Vaupel P. Hypoxic cervical cancers with low apoptotic index are highly aggressive. Cancer Res 1999;59:4525-8. 120. Zhong H, Chiles K, Feldser D, et al. Modulation of hypoxia-inducible factor 1alpha expression by the epidermal growth factor/phosphatidylinositol 3-kinase/PTEN/AKT/FRAP pathway in human prostate cancer cells: implications for tumor angiogenesis and therapeutics. Cancer Res 2000;60:1541-5. 121. Zundel W, Schindler C, Haas-Kogan D, et al. Loss of PTEN facilitates HIF-1-mediated gene expression. Genes Dev 2000;14:391-6. 122. Laughner E, Taghavi P, Chiles K, Mahon PC, Semenza GL. HER2 (neu) signaling increases the rate of hypoxia-inducible factor 1alpha (HIF-1alpha) synthesis: novel mechanism for HIF-1-mediated vascular endothelial growth factor expression. Mol Cell Biol 2001;21:3995-4004. 123. Fukuda R, Hirota K, Fan F, Jung YD, Ellis LM, Semenza GL. Insulin-like growth factor 1 induces hypoxia-inducible factor 1-mediated vascular endothelial growth factor expression, which is dependent on MAP kinase and phosphatidylinositol 3-kinase signaling in colon cancer cells. J Biol Chem 2002;277:38205-11. 124. Wang GL, Jiang BH, Semenza GL. Effect of protein kinase and phosphatase inhibitors on expression of hypoxia-inducible factor 1. Biochem Biophys Res Commun 1995;216:669-75. 125. Schofield CJ, Ratcliffe PJ. Oxygen sensing by HIF hydroxylases. Nat Rev Mol Cell Biol 2004;5:343-54. 126. Li H, Ko HP, Whitlock JP. Induction of phosphoglycerate kinase 1 gene expression by hypoxia. Roles of Arnt and HIF1alpha. J Biol Chem 1996;271:21262-7. 127. Jiang BH, Rue E, Wang GL, Roe R, Semenza GL. Dimerization, DNA binding, and transactivation properties of hypoxia-inducible factor 1. J Biol Chem 1996;271:17771-8. 128. Ruas JL, Poellinger L, Pereira T. Functional analysis of hypoxia-inducible factor-1 alpha-mediated transactivation. Identification of amino acid residues critical for transcriptional activation and/or interaction with CREB-binding protein. J Biol Chem 2002;277:38723-30. 129. Lando D, Gorman JJ, Whitelaw ML, Peet DJ. Oxygen-dependent regulation of hypoxia-inducible factors by prolyl and asparaginyl hydroxylation. Eur J Biochem 2003;270:781-90. 130. Makino Y, Cao R, Svensson K, et al. Inhibitory PAS domain protein is a negative regulator of hypoxia-inducible gene expression. Nature 2001;414:550-4. 131. Huang LE, Arany Z, Livingston DM, Bunn HF. Activation of hypoxia-inducible transcription factor depends primarily upon redox-sensitive stabilization of its alpha subunit. J Biol Chem 1996;271:32253-9. 132. Kallio PJ, Pongratz I, Gradin K, McGuire J, Poellinger L. Activation of hypoxia-inducible factor 1alpha: posttranscriptional regulation and conformational change by recruitment of the Arnt transcription factor. Proc Natl Acad Sci U S A 1997;94:5667-72. 133. Jewell UR, Kvietikova I, Scheid A, Bauer C, Wenger RH, Gassmann M. Induction of HIF-1alpha in response to hypoxia is instantaneous. FASEB J 2001;15:1312-4. 134. Hon WC, Wilson MI, Harlos K, et al. Structural basis for the recognition of hydroxyproline in HIF-1 alpha by pVHL. Nature 2002;417:975-8. 135. Min JH, Yang H, Ivan M, Gertler F, Kaelin WG, Jr., Pavletich NP. Structure of an HIF-1alpha -pVHL complex: hydroxyproline recognition in signaling. Science 2002;296:1886-9. 136. Jeong JW, Bae MK, Ahn MY, et al. Regulation and destabilization of HIF-1alpha by ARD1-mediated acetylation. Cell 2002;111:709-20. 137. Tanimoto K, Makino Y, Pereira T, Poellinger L. Mechanism of regulation of the hypoxia-inducible factor-1 alpha by the von Hippel-Lindau tumor suppressor protein. EMBO J 2000;19:4298-309. 138. Zelzer E, Levy Y, Kahana C, Shilo BZ, Rubinstein M, Cohen B. Insulin induces transcription of target genes through the hypoxia-inducible factor HIF-1alpha/ARNT. EMBO J 1998;17:5085-94. 139. Feldser D, Agani F, Iyer NV, Pak B, Ferreira G, Semenza GL. Reciprocal positive regulation of hypoxia-inducible factor 1alpha and insulin-like growth factor 2. Cancer Res 1999;59:3915-8. 140. Hellwig-Burgel T, Rutkowski K, Metzen E, Fandrey J, Jelkmann W. Interleukin-1beta and tumor necrosis factor-alpha stimulate DNA binding of hypoxia-inducible factor-1. Blood 1999;94:1561-7. 141. Richard DE, Berra E, Pouyssegur J. Nonhypoxic pathway mediates the induction of hypoxia-inducible factor 1alpha in vascular smooth muscle cells. J Biol Chem 2000;275:26765-71. 142. Gorlach A, Diebold I, Schini-Kerth VB, et al. Thrombin activates the hypoxia-inducible factor-1 signaling pathway in vascular smooth muscle cells: Role of the p22(phox)-containing NADPH oxidase. Circ Res 2001;89:47-54. 143. Haddad JJ, Land SC. A non-hypoxic, ROS-sensitive pathway mediates TNF-alpha-dependent regulation of HIF-1alpha. FEBS Lett 2001;505:269-74. 144. Stiehl DP, Jelkmann W, Wenger RH, Hellwig-Burgel T. Normoxic induction of the hypoxia-inducible factor 1alpha by insulin and interleukin-1beta involves the phosphatidylinositol 3-kinase pathway. FEBS Lett 2002;512:157-62. 145. Zhong H, De Marzo AM, Laughner E, et al. Overexpression of hypoxia-inducible factor 1alpha in common human cancers and their metastases. Cancer Res 1999;59:5830-5. 146. Talks KL, Turley H, Gatter KC, et al. The expression and distribution of the hypoxia-inducible factors HIF-1alpha and HIF-2alpha in normal human tissues, cancers, and tumor-associated macrophages. Am J Pathol 2000;157:411-21. 147. Aebersold DM, Burri P, Beer KT, et al. Expression of hypoxia-inducible factor-1alpha: a novel predictive and prognostic parameter in the radiotherapy of oropharyngeal cancer. Cancer Res 2001;61:2911-6. 148. Unruh A, Ressel A, Mohamed HG, et al. The hypoxia-inducible factor-1 alpha is a negative factor for tumor therapy. Oncogene 2003;22:3213-20. 149. Sun X, Kanwar JR, Leung E, Lehnert K, Wang D, Krissansen GW. Gene transfer of antisense hypoxia inducible factor-1 alpha enhances the therapeutic efficacy of cancer immunotherapy. Gene Ther 2001;8:638-45. 150. Kung AL, Wang S, Klco JM, Kaelin WG, Livingston DM. Suppression of tumor growth through disruption of hypoxia-inducible transcription. Nat Med 2000;6:1335-40. 151. Isaacs JS, Jung YJ, Mimnaugh EG, Martinez A, Cuttitta F, Neckers LM. Hsp90 regulates a von Hippel Lindau-independent hypoxia-inducible factor-1 alpha-degradative pathway. J Biol Chem 2002;277:29936-44. 152. Mabjeesh NJ, Post DE, Willard MT, et al. Geldanamycin induces degradation of hypoxia-inducible factor 1alpha protein via the proteosome pathway in prostate cancer cells. Cancer Res 2002;62:2478-82. 153. Zagzag D, Nomura M, Friedlander DR, et al. Geldanamycin inhibits migration of glioma cells in vitro: a potential role for hypoxia-inducible factor (HIF-1alpha) in glioma cell invasion. J Cell Physiol 2003;196:394-402. 154. Yeo EJ, Chun YS, Cho YS, et al. YC-1: a potential anticancer drug targeting hypoxia-inducible factor 1. J Natl Cancer Inst 2003;95:516-25. 155. Dachs GU, Patterson AV, Firth JD, et al. Targeting gene expression to hypoxic tumor cells. Nat Med 1997;3:515-20. 156. Lemmon MJ, van Zijl P, Fox ME, et al. Anaerobic bacteria as a gene delivery system that is controlled by the tumor microenvironment. Gene Ther 1997;4:791-6. 157. Harris AL. von Hippel-Lindau syndrome: target for anti-vascular endothelial growth factor (VEGF) receptor therapy. Oncologist 2000;5 Suppl 1:32-6. 158. Taunton J, Hassig CA, Schreiber SL. A mammalian histone deacetylase related to the yeast transcriptional regulator Rpd3p. Science 1996;272:408-11. 159. Bolden JE, Peart MJ, Johnstone RW. Anticancer activities of histone deacetylase inhibitors. Nat Rev Drug Discov 2006;5:769-84. 160. Struhl K. Histone acetylation and transcriptional regulatory mechanisms. Genes Dev 1998;12:599-606. 161. Pazin MJ, Kadonaga JT. What's up and down with histone deacetylation and transcription? Cell 1997;89:325-8. 162. Jenuwein T, Allis CD. Translating the histone code. Science 2001;293:1074-80. 163. Maison C, Bailly D, Peters AH, et al. Higher-order structure in pericentric heterochromatin involves a distinct pattern of histone modification and an RNA component. Nat Genet 2002;30:329-34. 164. Torchia J, Glass C, Rosenfeld MG. Co-activators and co-repressors in the integration of transcriptional responses. Curr Opin Cell Biol 1998;10:373-83. 165. Vigushin DM, Coombes RC. Histone deacetylase inhibitors in cancer treatment. Anticancer Drugs 2002;13:1-13. 166. Lin HY, Chen CS, Lin SP, Weng JR. Targeting histone deacetylase in cancer therapy. Med Res Rev 2006;26:397-413. 167. Liu T, Kuljaca S, Tee A, Marshall GM. Histone deacetylase inhibitors: multifunctional anticancer agents. Cancer Treat Rev 2006;32:157-65. 168. Gregoretti IV, Lee YM, Goodson HV. Molecular evolution of the histone deacetylase family: functional implications of phylogenetic analysis. J Mol Biol 2004;338:17-31. 169. Glozak MA, Sengupta N, Zhang X, Seto E. Acetylation and deacetylation of non-histone proteins. Gene 2005;363:15-23. 170. Marks PA, Dokmanovic M. Histone deacetylase inhibitors: discovery and development as anticancer agents. Expert Opin Investig Drugs 2005;14:1497-511. 171. Rosato RR, Grant S. Histone deacetylase inhibitors: insights into mechanisms of lethality. Expert Opin Ther Targets 2005;9:809-24. 172. Minucci S, Pelicci PG. Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer. Nat Rev Cancer 2006;6:38-51. 173. Zhao LJ, Subramanian T, Zhou Y, Chinnadurai G. Acetylation by p300 regulates nuclear localization and function of the transcriptional corepressor CtBP2. J Biol Chem 2006;281:4183-9. 174. Xu WS, Parmigiani RB, Marks PA. Histone deacetylase inhibitors: molecular mechanisms of action. Oncogene 2007;26:5541-52. 175. Glozak MA, Seto E. Histone deacetylases and cancer. Oncogene 2007;26:5420-32. 176. Iwabata H, Yoshida M, Komatsu Y. Proteomic analysis of organ-specific post-translational lysine-acetylation and -methylation in mice by use of anti-acetyllysine and -methyllysine mouse monoclonal antibodies. Proteomics 2005;5:4653-64. 177. Kim SC, Sprung R, Chen Y, et al. Substrate and functional diversity of lysine acetylation revealed by a proteomics survey. Mol Cell 2006;23:607-18. 178. Sambucetti LC, Fischer DD, Zabludoff S, et al. Histone deacetylase inhibition selectively alters the activity and expression of cell cycle proteins leading to specific chromatin acetylation and antiproliferative effects. J Biol Chem 1999;274:34940-7. 179. Richon VM, Sandhoff TW, Rifkind RA, Marks PA. Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene-associated histone acetylation. Proc Natl Acad Sci U S A 2000;97:10014-9. 180. Lagger G, O'Carroll D, Rembold M, et al. Essential function of histone deacetylase 1 in proliferation control and CDK inhibitor repression. EMBO J 2002;21:2672-81. 181. Halkidou K, Gaughan L, Cook S, Leung HY, Neal DE, Robson CN. Upregulation and nuclear recruitment of HDAC1 in hormone refractory prostate cancer. Prostate 2004;59:177-89. 182. Chang HH, Chiang CP, Hung HC, Lin CY, Deng YT, Kuo MY. Histone deacetylase 2 expression predicts poorer prognosis in oral cancer patients. Oral Oncol 2008. 183. Huang X, Guo B. Adenomatous polyposis coli determines sensitivity to histone deacetylase inhibitor-induced apoptosis in colon cancer cells. Cancer Res 2006;66:9245-51. 184. Song J, Noh JH, Lee JH, et al. Increased expression of histone deacetylase 2 is found in human gastric cancer. APMIS 2005;113:264-8. 185. Hrzenjak A, Moinfar F, Kremser ML, et al. Valproate inhibition of histone deacetylase 2 affects differentiation and decreases proliferation of endometrial stromal sarcoma cells. Mol Cancer Ther 2006;5:2203-10. 186. Zhu P, Martin E, Mengwasser J, Schlag P, Janssen KP, Gottlicher M. Induction of HDAC2 expression upon loss of APC in colorectal tumorigenesis. Cancer Cell 2004;5:455-63. 187. Ropero S, Fraga MF, Ballestar E, et al. A truncating mutation of HDAC2 in human cancers confers resistance to histone deacetylase inhibition. Nat Genet 2006;38:566-9. 188. Wilson AJ, Byun DS, Popova N, et al. Histone deacetylase 3 (HDAC3) and other class I HDACs regulate colon cell maturation and p21 expression and are deregulated in human colon cancer. J Biol Chem 2006;281:13548-58. 189. Westendorf JJ, Zaidi SK, Cascino JE, et al. Runx2 (Cbfa1, AML-3) interacts with histone deacetylase 6 and represses the p21(CIP1/WAF1) promoter. Mol Cell Biol 2002;22:7982-92. 190. Caslini C, Capo-chichi CD, Roland IH, Nicolas E, Yeung AT, Xu XX. Histone modifications silence the GATA transcription factor genes in ovarian cancer. Oncogene 2006;25:5446-61. 191. Subramanian C, Opipari AW, Jr., Bian X, Castle VP, Kwok RP. Ku70 acetylation mediates neuroblastoma cell death induced by histone deacetylase inhibitors. Proc Natl Acad Sci U S A 2005;102:4842-7. 192. Cohen HY, Lavu S, Bitterman KJ, et al. Acetylation of the C terminus of Ku70 by CBP and PCAF controls Bax-mediated apoptosis. Mol Cell 2004;13:627-38. 193. Johnstone RW, Licht JD. Histone deacetylase inhibitors in cancer therapy: is transcription the primary target? Cancer Cell 2003;4:13-8. 194. Ungerstedt JS, Sowa Y, Xu WS, et al. Role of thioredoxin in the response of normal and transformed cells to histone deacetylase inhibitors. Proc Natl Acad Sci U S A | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/44293 | - |
dc.description.abstract | 口腔癌為世界十大癌症之一,每年有超過五十萬的的病例被報導出來,釐清口腔癌的致病機轉為目前刻不容緩的課題。先前實驗室在口腔癌臨床病人的檢體中發現第二型組蛋白去乙醯化酶(Histone deacetylase 2, HDAC2)的表現與腫瘤組織的惡性度成正相關,因此本研究擬了解HDAC2在口腔癌癌化過程所扮演的角色及機轉。初步分析六株口腔癌細胞株,發現SAS細胞株的HDAC2有過量表現;HSC3細胞株表現量為最低。利用RNA干擾SAS細胞株HDAC2表現或於HSC3細胞株過量表現HDAC2的方法改變其表現量,並進行接下來的分析。 結果發現,SAS細胞的HDAC2被抑制以後,其生長速率下降、株落形成能力減弱、細胞週期發生G1停滯的現象,且其移行及侵犯組織的能力也明顯減弱; 然而,於HSC3細胞過量表現HDAC2後,其生長速率增加、株落形成能力增強,且其移行及侵犯能力更是明顯提升。 為了深入探討HDAC2於癌化的分子機轉中扮演的角色,利用人類基因晶片進行全面性的分析,發現有大量的缺氧型誘導基因同時被HDAC2調控。由進一步實驗結果得知,HDAC2會與HIF-1α結合,並利用去乙醯化的方式切掉K532上的乙醯基,避免其被透過VHL和ubiquitin調節機制標定而水解,進而維持HIF-1α在細胞中的穩定性。 大量累積在細胞質中的HIF-1α,會進行核轉移並活化缺氧誘導基因的轉錄,這些基因參與了腫瘤細胞的生存及轉移,包括: MMPs, Collagenases, CCLs, and ANGPTL4等。 其中,研究證實ANGPTL4的表現量確實經由HDAC2-HIF-1α的轉錄活化路徑所調控,且ANGPTL4也參與了口腔癌細胞的移行與侵犯。 原位(buccal mucosa)接種腫瘤細胞的動物模式中,抑制HDAC2的腫瘤生長速率較慢且淋巴結轉移的發生率較低; 然而,HDAC2過量表現的腫瘤生長速率較快,且發生嚴重的惡性淋巴結轉移。 本研究初步釐清了HDAC2在腫瘤組織發展中所扮演的角色,並期待研發出專一性HDAC2與HIF-1α的口腔癌治療策略。 | zh_TW |
dc.description.abstract | Oral squamous-cell carcinoma (OSCC) is one of the 10 most frequent cancers worldwide with more than half a million patients being diagnosed each year. Based on our previous study, over 70 % OSCC patients with HDAC2 over-expression were founded. Therefore, the roles of HDAC2 in tumorigenesis were elucidated in this study. We first screened six oral cancer cell lines and found that SAS cells with high expression of HDAC2 but HSC3 cells with low expression. Accordingly, HDAC2 knockdown stable line in SAS and HDAC over-expression stable line in HSC3 were established. SAS cells with HDAC2 knockdown showed slow growth rate, weak colony forming ability, and low metastatic potential in vitro. In contrast, HSC3 cells with HDAC2 over-expression presented fast growth rate, strong colony forming ability, and high metastatic potential in vitro. To illuminate the molecular mechanisms of HDAC2, we performed the whole human genome microarray which displayed that abundant hypoxia-associated genes were regulated by HDAC2. An important molecular regulation was revealed: HDAC2 stabilized HIF-1α protein through deacetylaton of the acetyl group on lysine 532 residue at normoxia and then the deacetylated HIF-1α protein would evade the VHL-ubiquitin-mediated degradation pathway. Considerable HIF-1α proteins accumulated in cytoplasm and also translocated into nucleus for transcriptional activation of hypoxia-induced genes, including MMPs, Collagenases, CCLs, and ANGPTL4. These pro-metastatic proteins facilitated cell survival, migration, invasion, intrvasation, and extravasation have been studied. We further investigated that ANGPTL4 protein involved in tumor migration and invasion in vitro and also confirm that the transcriptional activation of ANGPTL4 was regulated through HDAC2-HIF-1α-mediated pathway. In orthptopic (buccal mucosa injection) animal model, SAS cells with HDAC2 knockdown were low tumorigenesis and weak lymph node metastasis compared with vector controls in vivo, whereas HSC3 cells with HDAC2 over-expression were strong ability for tumorigenesis, growth and high lymph node metastasis compared with controls. Finally, we elucidated the multiple roles of HDAC2 in tumorigenesis and metastatic progression. Targeting of HDAC2 and HIF-1α are a novel strategy for oral cancer therapy. | en |
dc.description.provenance | Made available in DSpace on 2021-06-15T02:49:25Z (GMT). No. of bitstreams: 1 ntu-98-R96450003-1.pdf: 9805620 bytes, checksum: 3aae3ac1a7ecdda419a9f83f81f545f8 (MD5) Previous issue date: 2009 | en |
dc.description.tableofcontents | INTRODUCTIONS...............................................................1
CHAPTER 1: ORAL CANCER.....................................................1 1.1 Epidemiology and Etiology...........................................1 1.2 Carcinogen Exposures and Molecular Pathology........................2 1.3 Diagnosis and Treatment.............................................3 1.4 Novel Therapies.....................................................4 CHAPTER 2: THE FRAMEWORK OF METASTASIS.....................................6 2.1 Origin of Cellular Heterogeneity......................................7 2.2 Pressures that select for an aggressive phenotype.....................8 2.3 Prerequisites for metastasis tumor-initiating capacity................9 2.4 Events Happen Beyond the Basement Membrane...........................12 2.5 Highways to Distant Organs: Angiogenesis and Intravasation...........13 2.6 Survival in Transit and Extravasation................................14 2.7 Organ-specific Colonization..........................................14 2.8 Recent Advances of Metastasis Studies in Head and Neck Cancer........15 CHAPTER 3: HYPOXIA-INDUCED MECHANISMS......................................17 3.1 HIF-1α Protein Synthesis............................................17 3.2 HIF-1 α and β Subunits.............................................18 3.3 Molecular Mechanism of HIF-1α Stability.............................19 3.4 The Target Genes of HIF-1............................................20 3.5 HIF-1 Targeted Therapies.............................................20 CHAPTER 4: HISTONE DEACETYLASE............................................22 4.1 Histone Deacetylase Family...........................................22 4.2 Classic Pathway: Chromatin Modifications.............................22 4.3 Novel View of HDAC Functions.........................................23 4.4 HDACs and Cancer: Cancer Initiation..................................24 4.5 HDACs, HDAC Inhibitors and Cancer: Metastasis Progression............26 4.6 HDACs and Hypoxia....................................................29 SPECIFIC AIMS..............................................................31 MATERIALS AND METHODS......................................................33 RESULTS....................................................................41 DISCUSSIONS................................................................57 FIGURES....................................................................66 TABLES....................................................................117 APPENDIX..................................................................119 REFERENCES................................................................136 | |
dc.language.iso | en | |
dc.title | 第二型去乙醯化蛋白質在口腔致癌機轉中扮演的角色 | zh_TW |
dc.title | The Roles of Histone Deacetylase 2 in Tumorigenesis of Oral Cancer | en |
dc.type | Thesis | |
dc.date.schoolyear | 97-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 蕭宏昇(Michael Hsiao),張正琪(Cheng-Chi Chang) | |
dc.subject.keyword | 口腔癌,第二型去乙醯化蛋白質,第一型缺氧誘導因子,惡性轉移, | zh_TW |
dc.subject.keyword | oral cancer,metastasis,HDAC2,HIF-1α,ANGPTL4, | en |
dc.relation.page | 151 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2009-08-06 | |
dc.contributor.author-college | 牙醫專業學院 | zh_TW |
dc.contributor.author-dept | 口腔生物科學研究所 | zh_TW |
顯示於系所單位: | 口腔生物科學研究所 |
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