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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 陳進庭(Chin-Tin Chen) | |
dc.contributor.author | Shih-Hsuan Hung | en |
dc.contributor.author | 洪士軒 | zh_TW |
dc.date.accessioned | 2021-06-13T06:06:26Z | - |
dc.date.available | 2016-08-04 | |
dc.date.copyright | 2011-08-04 | |
dc.date.issued | 2011 | |
dc.date.submitted | 2011-07-26 | |
dc.identifier.citation | 1. Reynolds, R.M., et al., Von Recklinghausen's neurofibromatosis: neurofibromatosis type 1. Lancet, 2003. 361(9368): p. 1552-4.
2. Wallace, M.R., et al., Type 1 neurofibromatosis gene: identification of a large transcript disrupted in three NF1 patients. Science, 1990. 249(4965): p. 181-6. 3. Cawthon, R.M., et al., A major segment of the neurofibromatosis type 1 gene: cDNA sequence, genomic structure, and point mutations. Cell, 1990. 62(1): p. 193-201. 4. Li, Y., et al., Genomic organization of the neurofibromatosis 1 gene (NF1). Genomics, 1995. 25(1): p. 9-18. 5. Bernards, A., et al., Complete human NF1 cDNA sequence: two alternatively spliced mRNAs and absence of expression in a neuroblastoma line. DNA Cell Biol, 1992. 11(10): p. 727-34. 6. Daston, M.M., et al., The protein product of the neurofibromatosis type 1 gene is expressed at highest abundance in neurons, Schwann cells, and oligodendrocytes. Neuron, 1992. 8(3): p. 415-428. 7. Riccardi, V.M. and J. Smirniotopoulos, Neurofibromatosis, Phenotype, Natural History, and Pathogenesis. Journal of Neuropathology & Experimental Neurology, 1992. 51(6): p. 658. 8. Carey, J.C., J.M. Laub, and B.D. Hall, Penetrance and variability in neurofibromatosis: a genetic study of 60 families. Birth Defects Orig Artic Ser, 1979. 15(5B): p. 271-81. 9. Upadhyaya, M. and D. Cooper, Neurofibromatosis Type 1 (NF1), Genetics, in Encyclopedic Reference of Genomics and Proteomics in Molecular Medicine. 2006, Springer Berlin Heidelberg. p. 1271-1275. 10. DeClue, J.E., B.D. Cohen, and D.R. Lowy, Identification and characterization of the neurofibromatosis type 1 protein product. Proceedings of the National Academy of Sciences, 1991. 88(22): p. 9914-9918. 11. Xu, G.F., et al., The catalytic domain of the neurofibromatosis type 1 gene product stimulates ras GTPase and complements ira mutants of S. cerevisiae. Cell, 1990. 63(4): p. 835-41. 12. Yunoue, S., et al., Neurofibromatosis type I tumor suppressor neurofibromin regulates neuronal differentiation via its GTPase-activating protein function toward Ras. J Biol Chem, 2003. 278(29): p. 26958-69. 13. Sawada, S.i., et al., Identification of NF1 mutations in both alleles of a dermal neurofibroma. Nat Genet, 1996. 14(1): p. 110-112. 14. National Institutes of Health Consensus Development Conference, Neurofibromatosis: Conference Statement. Arch Neurol, 1988. 45(5): p. 575-578. 15. Rose, V.M., Neurocutaneous syndromes. Mo Med, 2004. 101(2): p. 112-6. 16. Carey, J.C. and D.H. Viskochil, Neurofibromatosis type 1: A model condition for the study of the molecular basis of variable expressivity in human disorders. American Journal of Medical Genetics, 1999. 89(1): p. 7-13. 17. Martuza, R.L., et al., Melanin Macroglobules As a Cellular Marker of Neurofibromatosis: A Quantitative Study. J Investig Dermatol, 1985. 85(4): p. 347-350. 18. Scheithauer, B.W., J.M. Woodruff, and R.A. Erlandson, Tumors of the Peripheral Nervous System. Washington, DC: Armed Forces Institute of Pathology, 1999. 19. Evans, D.G., et al., Malignant peripheral nerve sheath tumours in neurofibromatosis 1. J Med Genet, 2002. 39(5): p. 311-4. 20. Cohen, B.H., A.M. Kaplan, and R.J. Packer, Management of Intracranial Neoplasms in Children with Neurofibromatosis Type 1 and 2. Pediatric Neurosurgery, 1990. 16(2): p. 66-72. 21. Stiller, C.A., J.M. Chessells, and M. Fitchett, Neurofibromatosis and childhood leukaemia/lymphoma: a population-based UKCCSG study. Br J Cancer, 1994. 70(5): p. 969-72. 22. Korf, B.R., Clinical features and pathobiology of neurofibromatosis 1. J Child Neurol, 2002. 17(8): p. 573-7; discussion 602-4, 646-51. 23. Listernick, R., et al., Optic pathway gliomas in children with neurofibromatosis 1: Consensus statement from the nf1 optic pathway glioma task force. Annals of Neurology, 1997. 41(2): p. 143-149. 24. Elefteriou, F., et al., Skeletal abnormalities in neurofibromatosis type 1: Approaches to therapeutic options. American Journal of Medical Genetics Part A, 2009. 149A(10): p. 2327-2338. 25. North, K.N., et al., Cognitive function and academic performance in neurofibromatosis. 1: consensus statement from the NF1 Cognitive Disorders Task Force. Neurology, 1997. 48(4): p. 1121-7. 26. Carmi, D., et al., Growth, puberty, and endocrine functions in patients with sporadic or familial neurofibromatosis type 1: a longitudinal study. Pediatrics, 1999. 103(6 Pt 1): p. 1257-62. 27. Friedman, J.M., et al., Cardiovascular disease in neurofibromatosis 1: report of the NF1 Cardiovascular Task Force. Genet Med, 2002. 4(3): p. 105-11. 28. Oderich, G.S., et al., Vascular abnormalities in patients with neurofibromatosis syndrome type I: clinical spectrum, management, and results. J Vasc Surg, 2007. 46(3): p. 475-484. 29. Pascual-Castroviejo, I., et al., Neurofibromatosis type 1 with external genitalia involvement: Presentation of 4 patients. Journal of pediatric surgery, 2008. 43(11): p. 1998-2003. 30. Fuller, C.E. and G.T. Williams, Gastrointestinal manifestations of type 1 neurofibromatosis (von Recklinghausen's disease). Histopathology, 1991. 19(1): p. 1-11. 31. Woodruff, J.M., Pathology of tumors of the peripheral nerve sheath in type 1 neurofibromatosis. Am J Med Genet, 1999. 89(1): p. 23-30. 32. Sanguinetti, C., et al., The ultrastructure of schwannoma and neurofibroma of the peripheral nerves. Ital J Orthop Traumatol, 1991. 17(2): p. 237-46. 33. Muir, D., et al., Tumorigenic properties of neurofibromin-deficient neurofibroma Schwann cells. Am J Pathol, 2001. 158(2): p. 501-13. 34. Le, L.Q. and L.F. Parada, Tumor microenvironment and neurofibromatosis type I: connecting the GAPs. Oncogene, 2007. 26(32): p. 4609-16. 35. Sheela, S., V.M. Riccardi, and N. Ratner, Angiogenic and invasive properties of neurofibroma Schwann cells. J Cell Biol, 1990. 111(2): p. 645-53. 36. Menon, A.G., et al., Chromosome 17p deletions and p53 gene mutations associated with the formation of malignant neurofibrosarcomas in von Recklinghausen neurofibromatosis. Proc Natl Acad Sci U S A, 1990. 87(14): p. 5435-9. 37. Nielsen, G.P., et al., Malignant Transformation of Neurofibromas in Neurofibromatosis 1 Is Associated with CDKN2A/p16 Inactivation. Am J Pathol, 1999. 155(6): p. 1879-1884. 38. DeClue, J.E., et al., Epidermal growth factor receptor expression in neurofibromatosis type 1-related tumors and NF1 animal models. J Clin Invest, 2000. 105(9): p. 1233-41. 39. Guha, A., et al., Ras-GTP levels are elevated in human NF1 peripheral nerve tumors. Oncogene, 1996. 12(3): p. 507-13. 40. Poyhonen, M., S. Niemela, and R. Herva, Risk of malignancy and death in neurofibromatosis. Arch Pathol Lab Med, 1997. 121(2): p. 139-43. 41. Ferner, R.E., et al., Guidelines for the diagnosis and management of individuals with neurofibromatosis 1. J Med Genet, 2007. 44(2): p. 81-8. 42. Widemann, B.C., et al., Phase I trial and pharmacokinetic study of the farnesyltransferase inhibitor tipifarnib in children with refractory solid tumors or neurofibromatosis type I and plexiform neurofibromas. J Clin Oncol, 2006. 24(3): p. 507-16. 43. Riccardi, V.M., Mast-cell stabilization to decrease neurofibroma growth. Preliminary experience with ketotifen. Arch Dermatol, 1987. 123(8): p. 1011-6. 44. Gupta, A., et al., Phase I study of thalidomide for the treatment of plexiform neurofibroma in neurofibromatosis 1. Neurology, 2003. 60(1): p. 130-2. 45. Riccardi, V.M., A controlled multiphase trial of ketotifen to minimize neurofibroma-associated pain and itching. Arch Dermatol, 1993. 129(5): p. 577-81. 46. Dougherty, H., Thomas J., Barbara W., et al., Photodynamic Therapy. Journal of the National Cancer Institute, 1998. 90(12): p. 889-905. 47. Henderson, B.W., et al., Tumor destruction and kinetics of tumor cell death in two experimental mouse tumors following photodynamic therapy. Cancer Res, 1985. 45(2): p. 572-6. 48. Daniell, M.D. and J.S. Hill, A history of photodynamic therapy. Aust N Z J Surg, 1991. 61(5): p. 340-8. 49. Finsen, N., Phototherapy. 1901: Edward Arnold. 50. Roelandts, R., A new light on Niels Finsen, a century after his Nobel Prize. Photodermatol Photoimmunol Photomed, 2005. 21(3): p. 115-7. 51. Raab, O., Uber die Wirkung fluoreszierender Stoffe auf Infusorien. Zeitung Biol, 1900. 39: p. 524-526. 52. von Tappeiner, H. and A. Jesionek, Therapeutische versuche mit fluoreszierenden stoffen. Muench Med Wochenschr, 1903. 47: p. 2042–2044. 53. Hausmann, W., Die sensiblisierende Wirkung des Hematoporphyrins. Biochem Zeitung, 1911. 30: p. 276–316. 54. Lipson, R.L. and E.J. Baldes, The photodynamic properties of a particular hematoporphyrin derivative. Arch Dermatol, 1960. 82: p. 508-16. 55. Diamond, I., et al., Photodynamic therapy of malignant tumours. The Lancet, 1972. 300(7788): p. 1175-1177. 56. Dougherty, T.J., et al., Photoradiation therapy. II. Cure of animal tumors with hematoporphyrin and light. J Natl Cancer Inst, 1975. 55(1): p. 115-21. 57. Kelly, J.F., M.E. Snell, and M.C. Berenbaum, Photodynamic destruction of human bladder carcinoma. Br J Cancer, 1975. 31(2): p. 237-44. 58. Kelly, J.F. and M.E. Snell, Hematoporphyrin derivative: a possible aid in the diagnosis and therapy of carcinoma of the bladder. J Urol, 1976. 115(2): p. 150-1. 59. Dougherty, T.J., et al., Photoradiation therapy for the treatment of malignant tumors. Cancer Res, 1978. 38(8): p. 2628-35. 60. Triesscheijn, M., et al., Photodynamic Therapy in Oncology. The Oncologist, 2006. 11(9): p. 1034-1044. 61. Leman, J.A. and C.A. Morton, Photodynamic therapy: applications in dermatology. Expert Opin Biol Ther, 2002. 2(1): p. 45-53. 62. Soukos, N.S., et al., Targeted antimicrobial photochemotherapy. Antimicrob Agents Chemother, 1998. 42(10): p. 2595-601. 63. Henderson, B.W. and T.J. Dougherty, HOW DOES PHOTODYNAMIC THERAPY WORK? Photochemistry and Photobiology, 1992. 55(1): p. 145-157. 64. Dolmans, D.E., D. Fukumura, and R.K. Jain, Photodynamic therapy for cancer. Nat Rev Cancer, 2003. 3(5): p. 380-7. 65. Sharman, W.M., C.M. Allen, and J.E. van Lier, Photodynamic therapeutics: basic principles and clinical applications. Drug Discovery Today, 1999. 4(11): p. 507-517. 66. Moan, J. and K. Berg, The photodegradation of porphyrins in cells can be used to estimate the lifetime of singlet oxygen. Photochemistry and Photobiology, 1991. 53(4): p. 549-553. 67. Foote, C.S., Definition of type I and type II photosensitized oxidation. Photochem Photobiol, 1991. 54(5): p. 659. 68. Meyer–Betz, F., Untersuchungen uber die biologische photodynamische Wirkung des Hematoporphyrins und anderer Derivative des Blut und Galenafarbstoffs. Dtsch Arch Klin, 1913. 112: p. 476–503. 69. Policard, A., Etudes sur les aspects offerts par des tumeurs experimentales examinees a la lumiere de Wood. Compt Rend Soc Biol, 1924. 91: p. 1432. 70. Schwartz, S.K., K. Abolon, and H. Vermund, Some relationships of porphyrins, X-rays and tumors. Univ Minn Med Bull, 1955. 27: p. 7-8. 71. Lipson, R.L., E.J. Baldes, and A.M. Olsen, Hematoporphyrin derivative: a new aid for endoscopic detection of malignant disease. J Thorac Cardiovasc Surg, 1961. 42: p. 623-9. 72. QLT Phototherapeutics Inc, Canadian health protection branch approves Photofrin for treatment of esophageal cancer. Press Release, 1995. 73. Berenbaum, M.C., R. Bonnett, and P.A. Scourides, In vivo biological activity of the components of haematoporphyrin derivative. Br J Cancer, 1982. 45(4): p. 571-81. 74. Berenbaum, M.C., G.W. Hall, and A.D. Hoyes, Cerebral photosensitisation by haematoporphyrin derivative. Evidence for an endothelial site of action. Br J Cancer, 1986. 53(1): p. 81-9. 75. Wan, S., et al., Transmittance of non-ionizing radiation in human tissue. Photochemistry and Photobiology, 1981. 34(6): p. 679-681. 76. Detty, M.R., S.L. Gibson, and S.J. Wagner, Current Clinical and Preclinical Photosensitizers for Use in Photodynamic Therapy. Journal of Medicinal Chemistry, 2004. 47(16): p. 3897-3915. 77. Oleinick, N.L. and H.H. Evans, The Photobiology of Photodynamic Therapy: Cellular Targets and Mechanisms. Radiation Research, 1998. 150(5s): p. S146-S156. 78. Wilson, B., M. Patterson, and L. Lilge, Implicit and explicit dosimetry in photodynamic therapy: a New paradigm. Lasers in Medical Science, 1997. 12(3): p. 182-199. 79. Castano, A.P., P. Mroz, and M.R. Hamblin, Photodynamic therapy and anti-tumour immunity. Nat Rev Cancer, 2006. 6(7): p. 535-545. 80. DrugBank. Aminolevulinic acid. Available from: http://www.drugbank.ca/drugs/DB00855. 81. Peng, Q., et al., 5-Aminolevulinic acid-based photodynamic therapy: principles and experimental research. Photochem Photobiol, 1997. 65(2): p. 235-51. 82. Novo, M., G. H tmann, and H. Diddens, Chemical instability of 5-aminolevulinic acid used in the fluorescence diagnosis of bladder tumours. Journal of Photochemistry and Photobiology B: Biology, 1996. 34(2-3): p. 143-148. 83. Elfsson, B., et al., Stability of 5-aminolevulinic acid in aqueous solution. Eur J Pharm Sci, 1999. 7(2): p. 87-91. 84. Shemin, D. and C.S. Russell, d-Aminolevulinic acid, its role in the biosynthesis of porphyrins and purines. Journal of the American Chemical Society, 1953. 75(19): p. 4873-4874. 85. Phillips, J.D. and J.P. Kushner, The heme biosynthesis pathway and clinical manifestations of abnormal function. Curr Protoc Toxicol, 2001. Chapter 8: p. Unit 8 1. 86. Yamamoto, M., et al., Structure, turnover, and heme-mediated suppression of the level of mRNA encoding rat liver delta-aminolevulinate synthase. J Biol Chem, 1988. 263(31): p. 15973-9. 87. Lang, K., et al., Aminolevulinic acid: pharmacological profile and clinical indication. Expert Opin Investig Drugs, 2001. 10(6): p. 1139-56. 88. Gibson, S.L., et al., Relationship of delta-aminolevulinic acid-induced protoporphyrin IX levels to mitochondrial content in neoplastic cells in vitro. Biochem Biophys Res Commun, 1999. 265(2): p. 315-21. 89. Heyerdahl, H., et al., Pharmacokinetic studies on 5-aminolevulinic acid-induced protoporphyrin IX accumulation in tumours and normal tissues. Cancer Lett, 1997. 112(2): p. 225-31. 90. McGivan, J.D., Rat hepatoma cells express novel transport systems for glutamine and glutamate in addition to those present in normal rat hepatocytes. Biochem J, 1998. 330 ( Pt 1): p. 255-60. 91. Hilf, R., J.J. Havens, and S.L. Gibson, Effect of 5-AmJnolevulinic Acid on Protoporphyrin IX Accumulation in Tumor Cells Transfected with Plasmids Containing Porphobilinogen Deaminase DNA. Photochemistry and Photobiology, 1999. 70(3): p. 334-340. 92. van Hillegersberg, R., et al., Selective accumulation of endogenously produced porphyrins in a liver metastasis model in rats. Gastroenterology, 1992. 103: p. 647-51. 93. Morton, C.A., et al., Guidelines for topical photodynamic therapy: report of a workshop of the British Photodermatology Group. Br J Dermatol, 2002. 146(4): p. 552-67. 94. Brennan, M.J. and R.C. Cantrill, The effect of delta-aminolaevulinic acid on the uptake and efflux of [3H]GABA in rat brain synaptosomes. J Neurochem, 1979. 32(6): p. 1781-6. 95. Percy, V.A., M.C. Lamm, and J.J. Taljaard, delta-Aminolaevulinic acid uptake, toxicity, and effect on [14C]gamma-aminobutyric acid uptake into neurons and glia in culture. J Neurochem, 1981. 36(1): p. 69-76. 96. Bermúdez Moretti, M., et al., d-Aminolevulinic acid uptake is mediated by the g-aminobutyric acid-specific permease UGA4. Cellular and Molecular Biology, 1996. 42: p. 519–523. 97. Christensen, H.N., On the strategy of kinetic discrimination of amino acid transport systems. J Membr Biol, 1985. 84(2): p. 97-103. 98. Stevens, B.R., J.D. Kaunitz, and E.M. Wright, Intestinal transport of amino acids and sugars: advances using membrane vesicles. Annu Rev Physiol, 1984. 46: p. 417-33. 99. Rud, E., et al., 5-aminolevulinic acid, but not 5-aminolevulinic acid esters, is transported into adenocarcinoma cells by system BETA transporters. Photochem Photobiol, 2000. 71(5): p. 640-7. 100. Palacín, M., et al., Molecular biology of mammalian plasma membrane amino acid transporters. Physiol Rev, 1998. 78(4): p. 969-1054. 101. Bermudez Moretti, M., et al., Delta-Aminolevulinic acid transport in murine mammary adenocarcinoma cells is mediated by beta transporters. Br J Cancer, 2002. 87(4): p. 471-4. 102. Langer, S., et al., Active and higher intracellular uptake of 5-aminolevulinic acid in tumors may be inhibited by glycine. J Invest Dermatol, 1999. 112(5): p. 723-8. 103. Nelson, H., S. Mandiyan, and N. Nelson, Cloning of the human brain GABA transporter. FEBS Lett, 1990. 269(1): p. 181-4. 104. Borden, L.A., et al., Cloning and expression of a betaine/GABA transporter from human brain. J Neurochem, 1995. 64(3): p. 977-84. 105. Borden, L.A., et al., Molecular heterogeneity of the gamma-aminobutyric acid (GABA) transport system. Cloning of two novel high affinity GABA transporters from rat brain. J Biol Chem, 1992. 267(29): p. 21098-104. 106. Borden, L.A., et al., Cloning of the human homologue of the GABA transporter GAT-3 and identification of a novel inhibitor with selectivity for this site. Receptors Channels, 1994. 2(3): p. 207-13. 107. Döring, F., et al., Delta-aminolevulinic acid transport by intestinal and renal peptide transporters and its physiological and clinical implications. J Clin Invest, 1998. 101(12): p. 2761-7. 108. Irie, M., et al., Recognition and transport characteristics of nonpeptidic compounds by basolateral peptide transporter in Caco-2 cells. J Pharmacol Exp Ther, 2001. 298(2): p. 711-7. 109. Novotny, A., et al., Mechanisms of 5-aminolevulinic acid uptake at the choroid plexus. J Neurochem, 2000. 75(1): p. 321-8. 110. Berroeta, L., et al., A randomized study of minimal curettage followed by topical photodynamic therapy compared with surgical excision for low-risk nodular basal cell carcinoma. Br J Dermatol, 2007. 157(2): p. 401-3. 111. Warloe, T., et al., Photodynamic therapy with 5-aminoolevulinic acid-induced porphyrins and DMSO/EDTA for basal cell carcinoma. Proc SPIE, 1995. 2371: p. 226-235. 112. Pierre, M., et al., Oleic Acid as Optimizer of the Skin Delivery of 5-Aminolevulinic Acid in Photodynamic Therapy. Pharmaceutical Research, 2006. 23(2): p. 360-366. 113. Goff, B.A., et al., Effects of photodynamic therapy with topical application of 5-aminolevulinic acid on normal skin of hairless guinea pigs. Journal of Photochemistry and Photobiology B: Biology, 1992. 15(3): p. 239-251. 114. Gaullier, J.-M., et al., Use of 5-Aminolevulinic Acid Esters to Improve Photodynamic Therapy on Cells in Culture. Cancer Research, 1997. 57(8): p. 1481-1486. 115. Uehlinger, P., et al., 5-Aminolevulinic acid and its derivatives: physical chemical properties and protoporphyrin IX formation in cultured cells. J Photochem Photobiol B, 2000. 54(1): p. 72-80. 116. Chang, S.-F., et al., Enhancement of 5-aminolevulinic acid-induced photodynamic therapy by a bioadhesive polymer. Journal of Dental Sciences. 5(1): p. 30-35. 117. Berg, K., et al., The influence of iron chelators on the accumulation of protoporphyrin IX in 5-aminolaevulinic acid-treated cells. Br J Cancer, 1996. 74(5): p. 688-97. 118. Blake, E. and A. Curnow, The Hydroxypyridinone Iron Chelator CP94 Can Enhance PpIX-induced PDT of Cultured Human Glioma Cells. Photochemistry and Photobiology. 86(5): p. 1154-1160. 119. Ohgari, Y., et al., Quinolone compounds enhance d-aminolevulinic acid-induced accumulation of protoporphyrin IX and photosensitivity of tumour cells. Journal of Biochemistry, 2011. 149(2): p. 153-160. 120. Sinha, A.K., et al., Methotrexate used in combination with aminolaevulinic acid for photodynamic killing of prostate cancer cells. Br J Cancer, 2006. 95(4): p. 485-495. 121. Anand, S., et al., Low-dose methotrexate enhances aminolevulinate-based photodynamic therapy in skin carcinoma cells in vitro and in vivo. Clin Cancer Res, 2009. 15(10): p. 3333-43. 122. Galluzzi, L., et al., Cell death modalities: classification and pathophysiological implications. Cell Death Differ, 2007. 14(7): p. 1237-43. 123. Sun, Y. and Z.L. Peng, Programmed cell death and cancer. Postgrad Med J, 2009. 85(1001): p. 134-40. 124. Festjens, N., T. Vanden Berghe, and P. Vandenabeele, Necrosis, a well-orchestrated form of cell demise: Signalling cascades, important mediators and concomitant immune response. Biochimica et Biophysica Acta (BBA) - Bioenergetics. 1757(9-10): p. 1371-1387. 125. Golstein, P. and G. Kroemer, Cell death by necrosis: towards a molecular definition. Trends in Biochemical Sciences, 2007. 32(1): p. 37-43. 126. Zakeri, Z. and R.A. Lockshin, Cell death during development. Journal of Immunological Methods, 2002. 265(1-2): p. 3-20. 127. Earnshaw, W.C., L.M. Martins, and S.H. Kaufmann, Mammalian caspases: structure, activation, substrates, and functions during apoptosis. Annual review of biochemistry, 1999. 68: p. 383-424. 128. Elmore, S., Apoptosis: A Review of Programmed Cell Death. Toxicologic Pathology, 2007. 35(4): p. 495-516. 129. Gozuacik, D. and A. Kimchi, Autophagy and Cell Death, in Current Topics in Developmental Biology, P.S. Gerald, Editor. 2007, Academic Press. p. 217-245. 130. Lum, J.J., R.J. DeBerardinis, and C.B. Thompson, Autophagy in metazoans: cell survival in the land of plenty. Nat Rev Mol Cell Biol, 2005. 6(6): p. 439-448. 131. Codogno, P. and A.J. Meijer, Autophagy and signaling: their role in cell survival and cell death. Cell Death Differ, 2005. 12(S2): p. 1509-1518. 132. Giuntini, F., et al., Quantitative determination of 5-aminolaevulinic acid and its esters in cell lysates by HPLC-fluorescence. J Chromatogr B Analyt Technol Biomed Life Sci, 2008. 875(2): p. 562-6. 133. Hilf, R., J.J. Havens, and S.L. Gibson, Effect of delta-aminolevulinic acid on protoporphyrin IX accumulation in tumor cells transfected with plasmids containing porphobilinogen deaminase DNA. Photochem Photobiol, 1999. 70(3): p. 334-40. 134. Taketani, S., Measurement of Ferrochelatase Activity, in Current Protocols in Toxicology. 2001, John Wiley & Sons, Inc. 135. Slee, E.A., et al., Benzyloxycarbonyl-Val-Ala-Asp (OMe) fluoromethylketone (Z-VAD.FMK) inhibits apoptosis by blocking the processing of CPP32. Biochem J, 1996. 315 ( Pt 1): p. 21-4. 136. Seglen, P.O. and P.B. Gordon, 3-Methyladenine: specific inhibitor of autophagic/lysosomal protein degradation in isolated rat hepatocytes. Proc Natl Acad Sci U S A, 1982. 79(6): p. 1889-92. 137. Greco, W.R., G. Bravo, and J.C. Parsons, The search for synergy: a critical review from a response surface perspective. Pharmacological Reviews, 1995. 47(2): p. 331-385. 138. Ingle, J.D.J. and S.R. Crouch, Spectrochemical analysis. 1988: Prentice Hall College Book Division. 139. Haylett, T. and L. Thilo, Endosome-lysosome fusion at low temperature. Journal of Biological Chemistry, 1991. 266(13): p. 8322-8327. 140. Zhu, D., et al., Brownian Diffusion and Surface Kinetics of Liposome and Viral Particle Uptake by Human Lung Cancer Cells In-Vitro. Annals of Biomedical Engineering, 2006. 34(10): p. 1573-1586. 141. Robbins, E., P.I. Marcus, and N.K. Gonatas, Dynamics of acridine orange-cell interaction. The Journal of Cell Biology, 1964. 21(1): p. 49-62. 142. Gadmar, O.B., et al., The stability of 5-aminolevulinic acid in solution. J Photochem Photobiol B, 2002. 67(3): p. 187-93. 143. 康繼之, BMVC 相關小分子於癌症的研究:癌症檢測與光動力治療, in 化學系博士論文. 2010, 國立清華大學. 144. Speelmans, G., et al., Transport Studies of Doxorubicin in Model Membranes Indicate a Difference in Passive Diffusion across and Binding at the Outer and Inner Leaflet of the Plasma Membrane. Biochemistry, 1994. 33(46): p. 13761-13768. 145. Correa Garcia, S., et al., Mechanistic studies on [delta]-aminolevulinic acid uptake and efflux in a mammary adenocarcinoma cell line. Br J Cancer, 2003. 89(1): p. 173-177. 146. van Gemert, J.C., M.C. Berenbaum, and G.H. Gijsbers, Wavelength and light-dose dependence in tumour phototherapy with haematoporphyrin derivative. Br J Cancer, 1985. 52(1): p. 43-9. 147. Grossweiner, L.I., PDT light dosimetry revisited. J Photochem Photobiol B, 1997. 38(2-3): p. 258-68. 148. KOLÁŘOVÁ, H., et al., In vitro Study of Reactive Oxygen Species Production during Photodynamic Therapy in Ultrasound-Pretreated Cancer Cells. Physiol Res, 2007. 56 (Suppl. 1): p. S27-S32. 149. Brodin, B., B. Steffansen, and C.U. Nielsen, Passive diffusion of drug substances: the concepts of flux and permeability. 2010. 150. Tsai, T., et al., ALA-PDT results in phenotypic changes and decreased cellular invasion in surviving cancer cells. Lasers in Surgery and Medicine, 2009. 41(4): p. 305-315. 151. Tsai, J.-C., et al., Reorganization of cytoskeleton induced by 5-aminolevulinic acid-mediated photodynamic therapy and its correlation with mitochondrial dysfunction. Lasers in Surgery and Medicine, 2005. 36(5): p. 398-408. 152. Sporn, M.B. and A.B. Roberts, Autocrine growth factors and cancer. Nature, 1985. 313(6005): p. 745-747. 153. Wu, S.M., et al., Protoporphyrin IX production and its photodynamic effects on glioma cells, neuroblastoma cells and normal cerebellar granule cells in vitro with 5-aminolevulinic acid and its hexylester. Cancer letters, 2003. 200(2): p. 123-131. 154. Plaetzer, K., et al., The Modes of Cell Death Induced by PDT: An Overview. Medical Laser Application, 2003. 18(1): p. 7-19. 155. Castano, A.P., T.N. Demidova, and M.R. Hamblin, Mechanisms in photodynamic therapy: part two—cellular signaling, cell metabolism and modes of cell death. Photodiagnosis and photodynamic therapy, 2005. 2(1): p. 1-23. 156. Steinbach, P., et al., Cellular fluorescence of the endogenous photosensitizer protoporphyrin IX following exposure to 5-aminolevulinic acid. Photochem Photobiol, 1995. 62(5): p. 887-95. 157. Runnels, J.M., et al., BPD-MA-mediated photosensitization in vitro and in vivo: cellular adhesion and [bgr]1 integrin expression in ovarian cancer cells. Br J Cancer, 1999. 80(7): p. 946-953. 158. Trivedi, N.S., et al., Quantitative Analysis of Pc 4 Localization in Mouse Lymphoma (LY-R) Cells via Double-label Confocal Fluorescence Microscopy. Photochemistry and Photobiology, 2000. 71(5): p. 634-639. 159. Karmakar, S., et al., 5-Aminolevulinic acid-based photodynamic therapy suppressed survival factors and activated proteases for apoptosis in human glioblastoma U87MG cells. Neurosci Lett, 2007. 415(3): p. 242-7. 160. Grebenova, D., et al., Mitochondrial and endoplasmic reticulum stress-induced apoptotic pathways are activated by 5-aminolevulinic acid-based photodynamic therapy in HL60 leukemia cells. J Photochem Photobiol B, 2003. 69(2): p. 71-85. 161. Noodt, B.B., et al., Apoptosis and necrosis induced with light and 5-aminolaevulinic acid-derived protoporphyrin IX. Br J Cancer, 1996. 74(1): p. 22-9. 162. Juknat, A.A., et al., Necrotic cell death induced by delta-aminolevulinic acid in mouse astrocytes. Protective role of melatonin and other antioxidants. J Pineal Res, 2003. 35(1): p. 1-11. 163. Ji, H.T., et al., 5-ALA mediated photodynamic therapy induces autophagic cell death via AMP-activated protein kinase. Mol Cancer, 2010. 9: p. 91. 164. Gerritsen, M.J., et al., Pretreatment to enhance protoporphyrin IX accumulation in photodynamic therapy. Dermatology, 2009. 218(3): p. 193-202. 165. Berg, K., et al., The influence of iron chelators on the accumulation of protoporphyrin IX in 5-aminolaevulinic acid-treated cells. Br J Cancer, 1996. 74(5): p. 688-697. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/34395 | - |
dc.description.abstract | 第一型神經纖維瘤病(neurofibromatosis type 1)是一種常見之神經性自體顯性遺傳疾病,由NF1基因突變所致。主要病徵為表皮上大小程度不一的神經纖維瘤(neurofibroma),且有機會發展成惡性神經纖維肉瘤(neurofibrosarcoma),除了造成生理上的病痛外,外觀上的不雅也嚴重影響患者的心理發展。目前,此病尚未發展出一套有效的治療方式,傳統的手術切除面臨的最大問題在於腫瘤細胞是交纏著周邊的正常細胞而生長,術後不僅造成正常神經的損傷,也會因清除不完全而產生腫瘤復發及轉移。在臨床研究上,五氨基酮戊酸之光動力治療(5-aminolevulinic acid-mediated photodynamic therapy, ALA-PDT)具有光感物質高度選擇性累積於腫瘤之特質,並透過局部範圍之光照進而產生單態氧及自由基專一地對腫瘤細胞造成破壞,引發細胞之死亡。同時,為了提升ALA-PDT的治療效率,本研究將人類神經纖維肉瘤細胞S462以ALA-PDT加上其他藥物進行合併處理,可觀察到細胞毒殺效果與單獨處理相比,其效果顯著提升且具有協同效應,而且對於正常細胞並不會造成嚴重傷害。另外,合併處理後的細胞存活率無法藉由細胞凋亡與細胞自噬的抑制而提升,同時在細胞內也觀察到PI染劑的出現,說明細胞壞死(necrosis)的發生。更值得注意的是,本研究成功地建構出一套有效對抗神經纖維肉瘤的混和型治療模式,而這一個模式也適用於其他腫瘤的治療,這象徵著未來將可以此調控機制作為藥物作用及臨床應用之新標的。 | zh_TW |
dc.description.abstract | Neurofibromatosis type 1 (NF1) is one of the most common neurogenetic disorders with a high incidence, 1/3000. It is an autosomal dominant disease caused by a mutation in NF1 gene. Benign neurofibromas appeared in varied sizes on the skin are the major clinical symptoms in patients with NF1, and around 10% of neurofibromas would transform into malignant peripheral nerve sheath tumors (also named neurofibrosarcomas) with poor prognosis. In addition to physical pains, marked cosmetic disfigurements also serve patients as psychological traumas. Presently, no efficient therapy is available except for surgical resection. However, after surgery, the functions of nervous system may be destroyed or tumor recurrence and metastasis may occur due to the close cellular association between tumor and normal cells as well as growth along the nerve itself in neurofibromas. 5-Aminolevulinic acid-mediated photodynamic therapy (ALA-PDT), which involved the photochemical reactions based on the interaction of photosensitizing agents, light energy, and oxygen, has become a remarkable modality in anti-tumor therapy. Since the higher selective accumulation of ALA-derived PpIX in tumor cells, topical illumination can specifically induce oxidative stress followed by cell death to tumors. In this study, we tested ALA-PDT in combination with other compound to investigate the cytotoxic effects, cell death modes, and action mechanisms in human neurofibrosarcoma S462 cells. Photodynamic killing effect on tumor cells was synergistically induced, however, without severe damage to normal cells after exposure to 635 nm light. There was no rescue effect in applying the inhibition of apoptosis and autophagy and propidium iodide (PI) was shown inside the treated cells as well, indicating that necrotic cell death might be the major process caused by this treated model. Significantly, in this study, these results suggest that ALA-PDT has the potential for the treatment of neurofibrosarcoma. | en |
dc.description.provenance | Made available in DSpace on 2021-06-13T06:06:26Z (GMT). No. of bitstreams: 1 ntu-100-R98B47408-1.pdf: 5562680 bytes, checksum: 617a90c7f7e82b224d0cebecbcd909ec (MD5) Previous issue date: 2011 | en |
dc.description.tableofcontents | 口試委員審定書 i
中文摘要 ii 英文摘要(Abstract) iii 誌謝 v 目錄 vi 表目錄 xii 圖目錄 xiii 縮寫表 xv 第一章 緒論 1 1.1第一型神經纖維瘤病(Neurofibromatosis type 1, NF1) 1 1.1.1 NF1基因 1 1.1.2 Neurofibromin蛋白質 2 1.1.3臨床診斷與病徵 2 1.1.4神經纖維瘤與神經纖維肉瘤 5 1.1.5治療方法 6 1.2光動力治療(Photodynamic therapy, PDT) 6 1.2.1發展起源 7 1.2.2作用原理與機制 8 1.2.3光感物質 9 1.2.4作用位置及其引發之細胞傷害 10 1.3五氨基酮戊酸(5-Aminolevulinic acid, ALA) 11 1.3.1物化與生化特性 11 1.3.2原血紅素生合成路徑(Heme biosynthetic pathway) 12 1.3.3臨床應用優勢 13 1.3.4細胞膜吸收機轉 14 1.3.4.1胺基酸輸送載體(Amino acid transporter) 14 1.3.4.2 System BETA輸送載體 15 1.3.4.3胜肽輸送載體(Peptide transporter) 16 1.3.5發展與改良 17 1.4細胞死亡機轉(Cell death mechanism) 18 1.4.1細胞壞死(Necrosis) 19 1.4.2細胞凋亡(Apoptosis) 19 1.4.3細胞自噬(Autophagy) 19 1.5研究動機與目的 20 1.6研究架構 22 第二章 材料與方法 23 2.1藥品與儀器 23 2.1.1藥品 23 2.1.2細胞培養耗材 25 2.1.3儀器 26 2.2細胞株(Cell line) 28 2.3細胞培養與繼代(Subculture) 29 2.4細胞解凍與冷凍(Cell thawing and cryopreservation) 30 2.5細胞計數(Cell counting) 31 2.6細胞處理 32 2.6.1光動力處理(PDT alone) 32 2.6.2藥物處理(Drug alone) 33 2.6.3合併處理(Combined treatments) 33 2.6.3.1後處理模式(Post-treatment;ALA-PDT → CX1) 33 2.6.3.2前處理模式(Pre-treatment;CX1 → ALA-PDT) 33 2.6.3.3共同處理模式(Co-treatment;ALA-PDT & CX1) 34 2.6.4細胞型態觀察 34 2.7細胞存活率檢測 34 2.7.1粒線體去氫酶活性分析(MTT assay) 34 2.7.2細胞群落形成分析(Colony formation assay) 35 2.8藥物含量分析(Intracellular content assay) 36 2.8.1 ALA含量試驗(ALA content assay) 36 2.8.1.1 ALA吸收試驗(ALA uptake assay) 36 2.8.1.2 ALA排出試驗(ALA efflux assay) 38 2.8.2 PpIX含量試驗(PpIX accumulation assay) 39 2.8.2.1細胞內PpIX含量測定 39 2.8.2.2 PpIX螢光影像 40 2.9酵素活性分析(Enzymatic activity assay) 40 2.9.1 Porphobilinogen deaminase(PBGD) 40 2.9.2 Ferrochelatase(FC) 41 2.10細胞死亡模式分析(Cell death mode assay) 42 2.10.1抑制劑前處理(Inhibitors pre-treatment) 43 2.10.1.1 Z-VAD-FMK 43 2.10.1.2 3-Methyladenine(3-MA) 43 2.10.2形態學染色(Morphological staining) 43 2.10.2.1 Propidium iodide(PI) 43 2.10.2.2 Hoechst 44 2.10.2.3 Monodansylcadaverine(MDC) 44 2.11統計分析(Statistical analyses) 45 2.11.1 Significance of differences 45 2.11.2 Synergistic effect analysis 45 第三章 結果 46 3.1 ALA-PDT及Compound X1對S462細胞造成之細胞毒殺效應 46 3.1.1 ALA-PDT單獨處理S462細胞可降低細胞存活率 46 3.1.2 CX1單獨處理S462細胞可降低細胞存活率 46 3.1.3以ALA-PDT合併CX1處理S462細胞可提升細胞毒殺之效果 47 3.1.3.1後處理模式無法進一步降低細胞存活率 47 3.1.3.2前處理模式可進一步降低細胞存活率 48 3.1.3.3共同處理模式可進一步降低細胞存活率 48 3.1.3.4共同處理模式具有最大提升細胞毒殺之效果 49 3.1.4共同處理模式可在其他腫瘤細胞產生類似之協同效應,相對於正常細胞並不會造成嚴重傷害 49 3.2 ALA-PDT及Compound X1對S462細胞引發之細胞死亡模式 50 3.2.1 ALA-PDT單獨處理S462細胞將導致細胞壞死的發生 51 3.2.2 CX1單獨處理S462細胞將導致細胞自噬的發生 52 3.2.3以ALA-PDT合併CX1處理S462細胞將導致細胞壞死的發生 52 3.3以ALA-PDT合併Compound X1產生協同效應之作用機制 53 3.3.1 CX1能促進ALA及PpIX於細胞內的累積 53 3.3.2 CX1不影響PpIX生成路徑中PBGD及FC之活性 55 3.3.3 CX1透過降低細胞內ALA的排出而增進ALA的累積 56 3.3.3.1 CX1不會提升ALA於溶液中之穩定性 56 3.3.3.2 ALA與CX1之間無明顯鍵結產生 56 3.3.3.3 CX1可能會影響ALA輸送載體-BETA transporter之活性 58 3.3.3.4 CX1能降低細胞內ALA的排出 59 第四章 討論 60 4.1 ALA-PDT及Compound X1對S462細胞造成之細胞毒殺效應 60 4.1.1 ALA-PDT單獨處理可降低S462細胞之存活情形 60 4.1.2 CX1單獨處理可降低S462細胞之存活情形 61 4.1.3前處理與共同處理模式可進一步降低S462細胞之存活情形 62 4.1.4共同處理模式不傷及正常細胞,且可對其他腫瘤細胞造成破壞 63 4.2 ALA-PDT及Compound X1對S462細胞引發之細胞死亡模式 64 4.2.1 ALA-PDT單獨處理將造成S462細胞之細胞壞死 64 4.2.2 CX1單獨處理將造成S462細胞之細胞自噬 66 4.2.3以ALA-PDT合併CX1處理將造成S462細胞之細胞壞死 66 4.3以ALA-PDT合併Compound X1產生協同效應之作用機制 67 4.3.1 CX1能促進S462細胞對ALA及PpIX於細胞內的累積 68 4.3.2 CX1能降低細胞內ALA的排出而提升ALA的累積 69 第五章 結論 71 5.1以ALA-PDT合併CX1處理神經纖維肉瘤細胞有顯著毒殺效應 71 5.2以ALA-PDT合併CX1處理神經纖維肉瘤細胞將引發細胞壞死 71 5.3 CX1透過減少細胞內ALA排出的機制來達到協同效應 72 5.4 未來工作與展望 72 參考文獻 129 | |
dc.language.iso | zh-TW | |
dc.title | 五氨基酮戊酸光動力治療用於第一型神經纖維瘤病之研究探討 | zh_TW |
dc.title | Investigation of 5-aminolevulinic acid-mediated photodynamic therapy in neurofibromatosis type 1 | en |
dc.type | Thesis | |
dc.date.schoolyear | 99-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 蔡翠敏(Tsuimin Tsai),黃慶璨(Ching-Tsan Huang),許瑞祥(Ruey-Shyang Hseu),李銘仁(Ming-Jen Lee) | |
dc.subject.keyword | 五氨基酮戊酸,Protoporphyrin IX,神經纖維肉瘤,細胞吸收與排出, | zh_TW |
dc.subject.keyword | 5-Aminolevulinic acid,Protoporphyrin IX,Neurofibrosarcoma,Cellular uptake and efflux, | en |
dc.relation.page | 161 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2011-07-26 | |
dc.contributor.author-college | 生命科學院 | zh_TW |
dc.contributor.author-dept | 生化科技學系 | zh_TW |
顯示於系所單位: | 生化科技學系 |
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