請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/10754
完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 周綠蘋教授(Lu-Ping Chow) | |
dc.contributor.author | Wan-Hsin Liu | en |
dc.contributor.author | 劉宛欣 | zh_TW |
dc.date.accessioned | 2021-05-20T21:55:50Z | - |
dc.date.available | 2015-09-09 | |
dc.date.available | 2021-05-20T21:55:50Z | - |
dc.date.copyright | 2010-09-09 | |
dc.date.issued | 2010 | |
dc.date.submitted | 2010-07-26 | |
dc.identifier.citation | 1. (2008). Are the number of cancer cases increasing or decreasing in the world? WHO Online Q&A. WHO.
2. Parkin, D.M., Bray, F., Ferlay, J., and Pisani, P. (2005). Global cancer statistics, 2002. CA Cancer J Clin 55, 74-108. 3. Lauren, P. (1965). The two histological main types of gastric carcinoma: diffuse and so-called intestinal-type carcinoma. An attempt at a histo-clincial classification. Acta Pathol Microbiol Scand 64, 31-49. 4. Kelley, J.R., and Duggan, J.M. (2003). Gastric cancer epidemiology and risk factors. J Clin Epidemiol 56, 1-9. 5. Crew, K.D., and Neugut, A.I. (2006). Epidemiology of gastric cancer. World J Gastroenterol 12, 354-362. 6. Powell, J., and McConkey, C.C. (1992). The rising trend in oesophageal adenocarcinoma and gastric cardia. Eur J Cancer Prev 1, 265-269. 7. Armstrong, R.W., and Borman, B. (1996). Trends in incidence rates of adenocarcinoma of the oesophagus and gastric cardia in New Zealand, 1978-1992. Int J Epidemiol 25, 941-947. 8. Hansen, S., Wiig, J.N., Giercksky, K.E., and Tretli, S. (1997). Esophageal and gastric carcinoma in Norway 1958-1992: incidence time trend variability according to morphological subtypes and organ subsites. Int J Cancer 71, 340-344. 9. Harrison, S.L., Goldacre, M.J., and Seagroatt, V. (1992). Trends in registered incidence of oesophageal and stomach cancer in the Oxford region, 1974-88. Eur J Cancer Prev 1, 271-274. 10. Levi, F., La Vecchia, C., and Te, V.C. (1990). Descriptive epidemiology of adenocarcinomas of the cardia and distal stomach in the Swiss Canton of Vaud. Tumori 76, 167-171. 11. Moller, H., and Jensen, O.M. (1987). [Trends in the occurrence of esophageal, cardial and stomach cancer in Denmark 1943-1982. Neoplasm statistics No. 19]. Ugeskr Laeger 149, 1904-1909. 12. Pera, M., Cameron, A.J., Trastek, V.F., Carpenter, H.A., and Zinsmeister, A.R. (1993). Increasing incidence of adenocarcinoma of the esophagus and esophagogastric junction. Gastroenterology 104, 510-513. 13. Thomas, R.J., Lade, S., Giles, G.G., and Thursfield, V. (1996). Incidence trends in oesophageal and proximal gastric carcinoma in Victoria. Aust N Z J Surg 66, 271-275. 14. Lagergren, J., Bergstrom, R., and Nyren, O. (1999). Association between body mass and adenocarcinoma of the esophagus and gastric cardia. Ann Intern Med 130, 883-890. 15. Hohenberger, P., and Gretschel, S. (2003). Gastric cancer. Lancet 362, 305-315. 16. Terry, P., Lagergren, J., Ye, W., Wolk, A., and Nyren, O. (2001). Inverse association between intake of cereal fiber and risk of gastric cardia cancer. Gastroenterology 120, 387-391. 17. (1997). Cancer incidence in five continents. Volume VII. IARC Sci Publ, i-xxxiv, 1-1240. 18. McMichael, A.J., McCall, M.G., Hartshorne, J.M., and Woodings, T.L. (1980). Patterns of gastro-intestinal cancer in European migrants to Australia: the role of dietary change. Int J Cancer 25, 431-437. 19. Stalnikowicz, R., and Benbassat, J. (1990). Risk of gastric cancer after gastric surgery for benign disorders. Arch Intern Med 150, 2022-2026. 20. Joossens, J.V., Hill, M.J., Elliott, P., Stamler, R., Lesaffre, E., Dyer, A., Nichols, R., and Kesteloot, H. (1996). Dietary salt, nitrate and stomach cancer mortality in 24 countries. European Cancer Prevention (ECP) and the INTERSALT Cooperative Research Group. Int J Epidemiol 25, 494-504. 21. Kono, S., and Hirohata, T. (1996). Nutrition and stomach cancer. Cancer Causes Control 7, 41-55. 22. Hsing, A.W., Hansson, L.E., McLaughlin, J.K., Nyren, O., Blot, W.J., Ekbom, A., and Fraumeni, J.F., Jr. (1993). Pernicious anemia and subsequent cancer. A population-based cohort study. Cancer 71, 745-750. 23. Oh, S.T., Cha, J.H., Shin, D.J., Yoon, S.K., and Lee, S.K. (2007). Establishment and characterization of an in vivo model for Epstein-Barr virus positive gastric carcinoma. J Med Virol 79, 1343-1348. 24. Sharara, A.I., Abdul-Baki, H., ElHajj, I., Kreidieh, N., and Kfoury Baz, E.M. (2006). Association of gastroduodenal disease phenotype with ABO blood group and Helicobacter pylori virulence-specific serotypes. Dig Liver Dis 38, 829-833. 25. Palli, D., Galli, M., Caporaso, N.E., Cipriani, F., Decarli, A., Saieva, C., Fraumeni, J.F., Jr., and Buiatti, E. (1994). Family history and risk of stomach cancer in Italy. Cancer Epidemiol Biomarkers Prev 3, 15-18. 26. Howson, C.P., Hiyama, T., and Wynder, E.L. (1986). The decline in gastric cancer: epidemiology of an unplanned triumph. Epidemiol Rev 8, 1-27. 27. Parsonnet, J. (1995). The incidence of Helicobacter pylori infection. Aliment Pharmacol Ther 9 Suppl 2, 45-51. 28. Barreto-Zuniga, R., Maruyama, M., Kato, Y., Aizu, K., Ohta, H., Takekoshi, T., and Bernal, S.F. (1997). Significance of Helicobacter pylori infection as a risk factor in gastric cancer: serological and histological studies. J Gastroenterol 32, 289-294. 29. Hansson, L.E., Engstrand, L., Nyren, O., Evans, D.J., Jr., Lindgren, A., Bergstrom, R., Andersson, B., Athlin, L., Bendtsen, O., and Tracz, P. (1993). Helicobacter pylori infection: independent risk indicator of gastric adenocarcinoma. Gastroenterology 105, 1098-1103. 30. Hu, P.J., Mitchell, H.M., Li, Y.Y., Zhou, M.H., and Hazell, S.L. (1994). Association of Helicobacter pylori with gastric cancer and observations on the detection of this bacterium in gastric cancer cases. Am J Gastroenterol 89, 1806-1810. 31. Kokkola, A., Valle, J., Haapiainen, R., Sipponen, P., Kivilaakso, E., and Puolakkainen, P. (1996). Helicobacter pylori infection in young patients with gastric carcinoma. Scand J Gastroenterol 31, 643-647. 32. Miehlke, S., Hackelsberger, A., Meining, A., von Arnim, U., Muller, P., Ochsenkuhn, T., Lehn, N., Malfertheiner, P., Stolte, M., and Bayerdorffer, E. (1997). Histological diagnosis of Helicobacter pylori gastritis is predictive of a high risk of gastric carcinoma. Int J Cancer 73, 837-839. 33. Shogo Kikuchi, O.W.T.N.T.N.O.K.T.K.Y.I.R.G.o.P.o.G.C.a.Y.A. (1995). Serum anti-Helicobacter pylori antibody and gastric carcinoma among young adults. Cancer 75, 2789-2793. 34. Sipponen, P., Kosunen, T.U., Valle, J., Riihela, M., and Seppala, K. (1992). Helicobacter pylori infection and chronic gastritis in gastric cancer. J Clin Pathol 45, 319-323. 35. (1994). IARC working group on the evaluation of carcinogenic risks to humans: some industrial chemicals. Lyon, 15-22 February 1994. IARC Monogr Eval Carcinog Risks Hum 60, 1-560. 36. Correa, P., and Houghton, J. (2007). Carcinogenesis of Helicobacter pylori. Gastroenterology 133, 659-672. 37. Marshall, B.J., and Warren, J.R. (1984). Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration. Lancet 1, 1311-1315. 38. Amieva, M.R., and El-Omar, E.M. (2008). Host-bacterial interactions in Helicobacter pylori infection. Gastroenterology 134, 306-323. 39. Blaser, M.J. (1993). Helicobacter pylori: microbiology of a 'slow' bacterial infection. Trends Microbiol 1, 255-260. 40. Haas, R., Meyer, T.F., and van Putten, J.P. (1993). Aflagellated mutants of Helicobacter pylori generated by genetic transformation of naturally competent strains using transposon shuttle mutagenesis. Mol Microbiol 8, 753-760. 41. Hazell, S.L., Lee, A., Brady, L., and Hennessy, W. (1986). Campylobacter pyloridis and gastritis: association with intercellular spaces and adaptation to an environment of mucus as important factors in colonization of the gastric epithelium. J Infect Dis 153, 658-663. 42. Leying, H., Suerbaum, S., Geis, G., and Haas, R. (1992). Cloning and genetic characterization of a Helicobacter pylori flagellin gene. Mol Microbiol 6, 2863-2874. 43. Tompkins, L.S., and Falkow, S. (1995). The new path to preventing ulcers. Science 267, 1621-1622. 44. Censini, S., Lange, C., Xiang, Z., Crabtree, J.E., Ghiara, P., Borodovsky, M., Rappuoli, R., and Covacci, A. (1996). cag, a pathogenicity island of Helicobacter pylori, encodes type I-specific and disease-associated virulence factors. Proc Natl Acad Sci U S A 93, 14648-14653. 45. Montecucco, C., and Rappuoli, R. (2001). Living dangerously: how Helicobacter pylori survives in the human stomach. Nat Rev Mol Cell Biol 2, 457-466. 46. Peek, R.M., Jr., Vaezi, M.F., Falk, G.W., Goldblum, J.R., Perez-Perez, G.I., Richter, J.E., and Blaser, M.J. (1999). Role of Helicobacter pylori cagA(+) strains and specific host immune responses on the development of premalignant and malignant lesions in the gastric cardia. Int J Cancer 82, 520-524. 47. Ernst, P.B., and Gold, B.D. (2000). The disease spectrum of Helicobacter pylori: the immunopathogenesis of gastroduodenal ulcer and gastric cancer. Annu Rev Microbiol 54, 615-640. 48. Everhart, J.E. (2000). Recent developments in the epidemiology of Helicobacter pylori. Gastroenterol Clin North Am 29, 559-578. 49. Miyaji, H., Azuma, T., Ito, S., Abe, Y., Gejyo, F., Hashimoto, N., Sugimoto, H., Suto, H., Ito, Y., Yamazaki, Y., et al. (2000). Helicobacter pylori infection occurs via close contact with infected individuals in early childhood. J Gastroenterol Hepatol 15, 257-262. 50. Lauren, P. (1965). The Two Histological Main Types of Gastric Carcinoma: Diffuse and So-Called Intestinal-Type Carcinoma. An Attempt at a Histo-Clinical Classification. Acta Pathol Microbiol Scand 64, 31-49. 51. Frenck, R.W., Jr., and Clemens, J. (2003). Helicobacter in the developing world. Microbes Infect 5, 705-713. 52. Klein, P.D., Gilman, R.H., Leon-Barua, R., Diaz, F., Smith, E.O., and Graham, D.Y. (1994). The epidemiology of Helicobacter pylori in Peruvian children between 6 and 30 months of age. Am J Gastroenterol 89, 2196-2200. 53. Peek, R.M., Jr. (2001). IV. Helicobacter pylori strain-specific activation of signal transduction cascades related to gastric inflammation. Am J Physiol Gastrointest Liver Physiol 280, G525-530. 54. Konturek, P.C., Konturek, S.J., Pierzchalski, P., Bielanski, W., Duda, A., Marlicz, K., Starzynska, T., and Hahn, E.G. (2001). Cancerogenesis in Helicobacter pylori infected stomach--role of growth factors, apoptosis and cyclooxygenases. Med Sci Monit 7, 1092-1107. 55. Backert, S., and Selbach, M. (2005). Tyrosine-phosphorylated bacterial effector proteins: the enemies within. Trends in Microbiology 13, 476-484. 56. Peek, R.M., Jr., and Blaser, M.J. (2002). Helicobacter pylori and gastrointestinal tract adenocarcinomas. Nat Rev Cancer 2, 28-37. 57. Morita, D., Ichikura, T., and Mochizuki, H. (2001). [The expression of PPAR gamma in gastric cancer]. Nippon Rinsho 59 Suppl 4, 595-597. 58. Karim, S., Habib, A., Levy-Toledano, S., and Maclouf, J. (1996). Cyclooxygenase-1 and -2 of endothelial cells utilize exogenous or endogenous arachidonic acid for transcellular production of thromboxane. J Biol Chem 271, 12042-12048. 59. Pairet, M., and Engelhardt, G. (1996). Distinct isoforms (COX-1 and COX-2) of cyclooxygenase: possible physiological and therapeutic implications. Fundam Clin Pharmacol 10, 1-17. 60. Chen, C.C., Sun, Y.T., Chen, J.J., and Chiu, K.T. (2000). TNF-alpha-induced cyclooxygenase-2 expression in human lung epithelial cells: involvement of the phospholipase C-gamma 2, protein kinase C-alpha, tyrosine kinase, NF-kappa B-inducing kinase, and I-kappa B kinase 1/2 pathway. J Immunol 165, 2719-2728. 61. Coyne, D.W., Nickols, M., Bertrand, W., and Morrison, A.R. (1992). Regulation of mesangial cell cyclooxygenase synthesis by cytokines and glucocorticoids. Am J Physiol 263, F97-102. 62. Fosslien, E. (2000). Biochemistry of cyclooxygenase (COX)-2 inhibitors and molecular pathology of COX-2 in neoplasia. Crit Rev Clin Lab Sci 37, 431-502. 63. Fu, J.Y., Masferrer, J.L., Seibert, K., Raz, A., and Needleman, P. (1990). The induction and suppression of prostaglandin H2 synthase (cyclooxygenase) in human monocytes. J Biol Chem 265, 16737-16740. 64. Geng, Y., Blanco, F.J., Cornelisson, M., and Lotz, M. (1995). Regulation of cyclooxygenase-2 expression in normal human articular chondrocytes. J Immunol 155, 796-801. 65. Lee, S.H., Soyoola, E., Chanmugam, P., Hart, S., Sun, W., Zhong, H., Liou, S., Simmons, D., and Hwang, D. (1992). Selective expression of mitogen-inducible cyclooxygenase in macrophages stimulated with lipopolysaccharide. J Biol Chem 267, 25934-25938. 66. Vane, J.R., Bakhle, Y.S., and Botting, R.M. (1998). Cyclooxygenases 1 and 2. Annu Rev Pharmacol Toxicol 38, 97-120. 67. Ulrich, C.M., Bigler, J., and Potter, J.D. (2006). Non-steroidal anti-inflammatory drugs for cancer prevention: promise, perils and pharmacogenetics. Nat Rev Cancer 6, 130-140. 68. Konturek, P.C., Konturek, S.J., and Brzozowski, T. (2006). Gastric cancer and Helicobacter pylori infection. J Physiol Pharmacol 57 Suppl 3, 51-65. 69. Konturek, P.C., Kania, J., Kukharsky, V., Ocker, S., Hahn, E.G., and Konturek, S.J. (2003). Influence of gastrin on the expression of cyclooxygenase-2, hepatocyte growth factor and apoptosis-related proteins in gastric epithelial cells. J Physiol Pharmacol 54, 17-32. 70. Ito, M., Tanaka, S., Maeda, M., Takamura, A., Tatsugami, M., Wada, Y., Matsumoto, Y., Yoshihara, M., Haruma, K., and Chayama, K. (2008). Role of the gastrin-gastrin receptor system in the expansive growth of human gastric neoplasms. Digestion 78, 163-170. 71. Guo, X.L., Wang, L.E., Du, S.Y., Fan, C.L., Li, L., Wang, P., and Yuan, Y. (2003). Association of cyclooxygenase-2 expression with Hp-cagA infection in gastric cancer. World J Gastroenterol 9, 246-249. 72. Iwamoto, J., Mizokami, Y., Takahashi, K., Matsuoka, T., and Matsuzaki, Y. (2008). The effects of cyclooxygenase2-prostaglandinE2 pathway on Helicobacter pylori-induced urokinase-type plasminogen activator system in the gastric cancer cells. Helicobacter 13, 174-182. 73. Yamac, D., Ayyildiz, T., Coskun, U., Akyurek, N., Dursun, A., Seckin, S., and Koybasioglu, F. (2008). Cyclooxygenase-2 expression and its association with angiogenesis, Helicobacter pylori, and clinicopathologic characteristics of gastric carcinoma. Pathol Res Pract 204, 527-536. 74. Chang, Y.J., Wu, M.S., Lin, J.T., and Chen, C.C. (2005). Helicobacter pylori-Induced invasion and angiogenesis of gastric cells is mediated by cyclooxygenase-2 induction through TLR2/TLR9 and promoter regulation. J Immunol 175, 8242-8252. 75. Shen, H., Sun, W.H., Xue, Q.P., Wu, J., Cheng, Y.L., Ding, G.X., Fu, H.Y., Tsuji, S., and Kawano, S. (2006). Influences of Helicobacter pylori on cyclooxygenase-2 expression and prostaglandinE2 synthesis in rat gastric epithelial cells in vitro. J Gastroenterol Hepatol 21, 754-758. 76. Kabir, S. (2009). Effect of Helicobacter pylori eradication on incidence of gastric cancer in human and animal models: underlying biochemical and molecular events. Helicobacter 14, 159-171. 77. Krysan, K., Merchant, F.H., Zhu, L., Dohadwala, M., Luo, J., Lin, Y., Heuze-Vourc'h, N., Pold, M., Seligson, D., Chia, D., et al. (2004). COX-2-dependent stabilization of survivin in non-small cell lung cancer. FASEB J 18, 206-208. 78. Yamamoto, H., Ngan, C.Y., and Monden, M. (2008). Cancer cells survive with survivin. Cancer Sci 99, 1709-1714. 79. Mita, A.C., Mita, M.M., Nawrocki, S.T., and Giles, F.J. (2008). Survivin: key regulator of mitosis and apoptosis and novel target for cancer therapeutics. Clin Cancer Res 14, 5000-5005. 80. Song, K.Y., Jung, C.K., Park, W.S., and Park, C.H. (2009). Expression of the antiapoptosis gene Survivin predicts poor prognosis of stage III gastric adenocarcinoma. Jpn J Clin Oncol 39, 290-296. 81. Chen, T., and Deng, C. (2008). Inhibitory effect of siRNA targeting survivin in gastric cancer MGC-803 cells. Int Immunopharmacol 8, 1006-1011. 82. Miao, G.Y., Lu, Q.M., and Zhang, X.L. (2007). Downregulation of survivin by RNAi inhibits growth of human gastric carcinoma cells. World J Gastroenterol 13, 1170-1174. 83. Pai, S.I., Lin, Y.Y., Macaes, B., Meneshian, A., Hung, C.F., and Wu, T.C. (2006). Prospects of RNA interference therapy for cancer. Gene Ther 13, 464-477. 84. Erkanli, S., Bolat, F., Kayaselcuk, F., Demirhan, B., and Kuscu, E. (2007). COX-2 and survivin are overexpressed and positively correlated in endometrial carcinoma. Gynecol Oncol 104, 320-325. 85. Lambropoulou, M., Papadopoulos, N., Tripsianis, G., Alexiadis, G., Pagonopoulou, O., Kiziridou, A., Liberis, V., Kakolyris, S., and Chatzaki, E. Co-expression of survivin, c-erbB2, and cyclooxygenase-2 (COX-2): prognostic value and survival of endometrial cancer patients. J Cancer Res Clin Oncol 136, 427-435. 86. Younis, T., Hache, K.D., Rayson, D., Dewar, R., Gray, S., and Barnes, P.J. (2009). Survivin and COX-2 expression in male breast carcinoma. Breast 18, 228-232. 87. Song, I.H., Kim, D.W., Shin, K.C., Shin, H.D., Yun, S.Y., Kim, S.B., Shin, J.E., Kim, H.J., and Kim, E.Y. (2008). [Down-regulation of survivin in growth inhibition of hepatoma cells induced by a selective cyclooxygenase-2 inhibitor]. Korean J Hepatol 14, 351-359. 88. Luo, S.M., Liu, R.D., Li, W.R., and Hou, J.H. (2009). [Survivin and COX-2 expressions in giant cell tumor of bone and their relation to the prognosis]. Nan Fang Yi Ke Da Xue Xue Bao 29, 156-159. 89. Athanassiadou, P., Grapsa, D., Athanassiades, P., Gonidi, M., Athanassiadou, A.M., Tsipis, A., and Patsouris, E. (2008). The prognostic significance of COX-2 and survivin expression in ovarian cancer. Pathol Res Pract 204, 241-249. 90. Yu, J., Leung, W.K., Ebert, M.P., Ng, E.K., Go, M.Y., Wang, H.B., Chung, S.C., Malfertheiner, P., and Sung, J.J. (2002). Increased expression of survivin in gastric cancer patients and in first degree relatives. Br J Cancer 87, 91-97. 91. Tomb, J.F., White, O., Kerlavage, A.R., Clayton, R.A., Sutton, G.G., Fleischmann, R.D., Ketchum, K.A., Klenk, H.P., Gill, S., Dougherty, B.A., et al. (1997). The complete genome sequence of the gastric pathogen Helicobacter pylori. Nature 388, 539-547. 92. Su, B., Ceponis, P.J., and Sherman, P.M. (2003). Cytoskeletal rearrangements in gastric epithelial cells in response to Helicobacter pylori infection. J Med Microbiol 52, 861-867. 93. Herrler, T., Leicht, S.F., Huber, S., Hermann, P.C., Schwarz, T.M., Kopp, R., and Heeschen, C. (2009). Prostaglandin E positively modulates endothelial progenitor cell homeostasis: an advanced treatment modality for autologous cell therapy. J Vasc Res 46, 333-346. 94. North, T.E., Goessling, W., Walkley, C.R., Lengerke, C., Kopani, K.R., Lord, A.M., Weber, G.J., Bowman, T.V., Jang, I.H., Grosser, T., et al. (2007). Prostaglandin E2 regulates vertebrate haematopoietic stem cell homeostasis. Nature 447, 1007-1011. 95. Angell, H. (2008). A study into the potential role of Survivin localization in resistance to drug-induced apoptosis. Bioscience Horizons 1, 85-91. 96. Connell, C.M., Colnaghi, R., and Wheatley, S.P. (2008). Nuclear survivin has reduced stability and is not cytoprotective. J Biol Chem 283, 3289-3296. 97. Qi, G., Tuncel, H., Aoki, E., Tanaka, S., Oka, S., Kaneko, I., Okamoto, M., Tatsuka, M., Nakai, S., and Shimamoto, F. (2009). Intracellular localization of survivin determines biological behavior in colorectal cancer. Oncol Rep 22, 557-562. 98. Li, X.D.-h.W.J.-d.J.B.Z.Y.-y.Z.F.-z.C. (2006). Cloning of survivin promoter and its specific transcriptional activities in gastric cancer cell line AGS. China Journal of Modern Medicine 16. 99. Chiou, S.K., and Mandayam, S. (2007). NSAIDs enhance proteasomic degradation of survivin, a mechanism of gastric epithelial cell injury and apoptosis. Biochem Pharmacol 74, 1485-1495. 100. Hunter, T. (2007). The age of crosstalk: phosphorylation, ubiquitination, and beyond. Mol Cell 28, 730-738. 101. Arora, V., Cheung, H.H., Plenchette, S., Micali, O.C., Liston, P., and Korneluk, R.G. (2007). Degradation of survivin by the X-linked inhibitor of apoptosis (XIAP)-XAF1 complex. J Biol Chem 282, 26202-26209. 102. Tu, S.P., Liston, P., Cui, J.T., Lin, M.C., Jiang, X.H., Yang, Y., Gu, Q., Jiang, S.H., Lum, C.T., Kung, H.F., et al. (2009). Restoration of XAF1 expression induces apoptosis and inhibits tumor growth in gastric cancer. Int J Cancer 125, 688-697. 103. Tu, S.P., Sun, Y.W., Cui, J.T., Zou, B., Lin, M.C., Gu, Q., Jiang, S.H., Kung, H.F., Korneluk, R.G., and Wong, B.C. Tumor suppressor XIAP-Associated factor 1 (XAF1) cooperates with tumor necrosis factor-related apoptosis-inducing ligand to suppress colon cancer growth and trigger tumor regression. Cancer 116, 1252-1263. 104. Chung, S.K., Lee, M.G., Ryu, B.K., Lee, J.H., Han, J., Byun, D.S., Chae, K.S., Lee, K.Y., Jang, J.Y., Kim, H.J., et al. (2007). Frequent alteration of XAF1 in human colorectal cancers: implication for tumor cell resistance to apoptotic stresses. Gastroenterology 132, 2459-2477. 105. Byun, D.S., Cho, K., Ryu, B.K., Lee, M.G., Kang, M.J., Kim, H.R., and Chi, S.G. (2003). Hypermethylation of XIAP-associated factor 1, a putative tumor suppressor gene from the 17p13.2 locus, in human gastric adenocarcinomas. Cancer Res 63, 7068-7075. 106. Liew, J.C., Tan, W.S., Alitheen, N.B., Chan, E.S., and Tey, B.T. Over-expression of the X-linked inhibitor of apoptosis protein (XIAP) delays serum deprivation-induced apoptosis in CHO-K1 cells. J Biosci Bioeng. 107. Hiscutt, E.L., Hill, D.S., Martin, S., Kerr, R., Harbottle, A., Birch-Machin, M., Redfern, C.P., Fulda, S., Armstrong, J.L., and Lovat, P.E. Targeting X-Linked Inhibitor of Apoptosis Protein to Increase the Efficacy of Endoplasmic Reticulum Stress-Induced Apoptosis for Melanoma Therapy. J Invest Dermatol. 108. Seeger, J.M., Brinkmann, K., Yazdanpanah, B., Haubert, D., Pongratz, C., Coutelle, O., Kronke, M., and Kashkar, H. Elevated XIAP expression alone does not confer chemoresistance. Br J Cancer 102, 1717-1723. 109. Kim, S.H., and Singh, S.V. p53-Independent apoptosis by benzyl isothiocyanate in human breast cancer cells is mediated by suppression of XIAP expression. Cancer Prev Res (Phila Pa) 3, 718-726. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/10754 | - |
dc.description.abstract | 胃癌是世界上最常見的癌症之一。目前最受科學家注意的是幽門螺旋桿菌感染而造成的胃癌。儘管近年來有許多研究著重於幽門螺旋桿菌其致病機轉的探討,幽門螺旋桿菌導致胃癌發生的詳細機制卻仍還不是完全清楚。由先前的研究指出,幽門螺旋桿菌的寄生將會導致宿主胃部黏膜的發炎,由目前的研究顯示其主要原因之一是二號環氧化酶 (COX-2) 被幽門螺旋桿菌誘導表現所致。二號環氧酶為一製造前列腺素 PGE2 之酵素,除了參與發炎反應外,尚有研究指出,COX-2 以及 PGE2 可能參與抗細胞凋亡反應,然而 COX-2 及 PGE2 是如何參與或調控抗細胞凋亡反應目前尚不清楚。本論文利用幽門螺旋桿菌感染胃上皮細胞 AGS 確立幽門螺旋桿菌的感染可以促進抗細胞凋亡分子「存活素」的大量表現,並發現 COX-2 及 PGE2 均參與減少存活素泛素化之調控,為更進一步研究 COX-2 對存活素之調控,本論文以 shRNA 或者選擇性抑制 COX-2 之藥物 Celecoxib 處理幽門螺旋桿菌感染之 AGS,均有促使 AGS 中存活素下降之趨勢,證明,幽門螺旋桿菌確可以透過 COX-2 的表達以及其下游分子 PGE2 之產生來抑制存活素的泛素化,並減少其降解,因此 COX-2 可能是透過其和其下游分子 PGE2 之作用來穩定存活素,進而行使抗細胞凋亡之功能。除此之外,為了探討存活素是否確實在細胞質中行抗細胞凋亡反應,本論文更使用螢光顯微鏡觀察存活素在細胞中之位置,可觀察到處理幽門螺旋桿菌後,存活素確有自細胞核移至細胞質之現象,因此存活素可能在幽門螺旋桿菌感染後行使抗細胞凋亡之功能。本論文首度證明了幽門螺旋桿菌確有透過 COX-2 以及PGE2 來穩定存活素之現象,並證明了幽門螺旋桿菌可以透過引起存活素在細胞中位置之改變,因此可以產生抗細胞凋亡反應,進而導致胃癌產生。 | zh_TW |
dc.description.abstract | Gastric cancer is one of the most common cancers and Helicobracter pylori (H. pylori) infection has been widely accepted as a major factor of gastric cancer. Although many efforts have been made to study H. pylori, the exact mechanisms of gastric carcinogenesis induced by H. pylori remain unclear. Past studies have reported that H. pylori infection results in the over-expression of cyclooxygenase-2 (COX-2). It has been reported that both COX-2 and its downstream factor PGE2 may be involved in the regulation of anti-apoptosis, but the exact mechanisms is unclear. This thesis shows that H. pylori infection not only induces the over-expression of COX-2 but also results in the over-expression of anti-apoptotic factor, survivin, in gastric epithelial cells, AGS. In addition, both COX-2 and PGE2 stabilize survivin by decreasing the ubiquitination of survivin. Moreover, a significant decrease of the amount of survin is observed when either the shRNA of COX-2 or the selective COX-2 inhibitor, celecoxib, is used to inhibit the COX-2 induced by H. pylori infection. These results show that H. pylori infection can induce a great amount of survivin by over-expressing COX-2 and PGE2, which stabilize survivin. In addition, by using immunofluorescent microscopy to examine the location of survivin, it is observed that survivin translocates from nucleus to cytoplasm after H. pylori infection. This result implies that H. pylori can change the location of survivin so that survivin could execute anti-apoptosis. To my best knowledge, this is the first work that shows the infection of H. pylori induces a great amount of survivin, which is stabilized by COX-2 and PGE2, and induces the translocation of survivin. | en |
dc.description.provenance | Made available in DSpace on 2021-05-20T21:55:50Z (GMT). No. of bitstreams: 1 ntu-99-R97442002-1.pdf: 2254825 bytes, checksum: 1bd45962e4bb4babd59957190d39e095 (MD5) Previous issue date: 2010 | en |
dc.description.tableofcontents | 摘要 iv
Abstract vi 縮寫 viii 第一章 導論 3 第一節 胃癌簡介 3 第二節 幽門螺旋桿菌 (Helicobacter pylor, H. pylori) 9 第三節 幽門螺旋桿菌所造成之宿主反應 (host response) 12 第四節 第二型環氧化酶與其下游分子和胃癌的發生 17 第五節 存活素與胃癌 20 第六節 本篇論文的研究目的 24 第二章 實驗材料 26 第三章 實驗方法 30 第一節 幽門螺旋桿菌與胃腺癌細胞的培養 30 第二節 幽門螺旋桿菌感染胃腺癌細胞 32 第三節 質體抽取 34 第四節 蛋白質分析法 36 第五節 螢光顯微鏡觀察 42 第四章 實驗結果 44 第一節 幽門螺旋桿菌感染 AGS 細胞促使存活素上升 44 第二節 COX-2 表現與存活素上升之關係 45 第三節 PGE2 表現與存活素上升之關係 48 第四節 幽門螺旋桿菌感染引起存活素位置之改變 49 第五節 幽門螺旋桿菌感染引起存活素上升的其它訊息路徑 50 第五章 討論 52 第一節 實驗方法討論 52 第二節 H. pylori所引起磷酸化訊息傳遞之改變 55 第三節 總結與未來展望 56 第六章 參考文獻 58 第七章 圖表與說明 68 附錄 80 | |
dc.language.iso | zh-TW | |
dc.title | 幽門螺旋桿菌感染誘導之胃上皮細胞抗細胞凋亡分子分析與機制探討 | zh_TW |
dc.title | Analysis of anti-apoptotic factors induced by Helicobacter pylori infection of gastric epithelial cells | en |
dc.type | Thesis | |
dc.date.schoolyear | 98-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 楊雅倩教授(Ya-Chien Yang),趙瑞益教授(Jui-I Chao),繆希椿教授(Shi-Chuen Miaw) | |
dc.subject.keyword | 幽門螺旋桿菌,胃癌,COX-2,存活素,抗細胞凋亡, | zh_TW |
dc.subject.keyword | Helicobacter pylori,gastric cancer,COX-2,survivin,anti-apoptosis, | en |
dc.relation.page | 80 | |
dc.rights.note | 同意授權(全球公開) | |
dc.date.accepted | 2010-07-26 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 生物化學暨分子生物學研究所 | zh_TW |
顯示於系所單位: | 生物化學暨分子生物學科研究所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-99-1.pdf | 2.2 MB | Adobe PDF | 檢視/開啟 |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。