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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 張玉芳(Julia Yu Fong Chang 張玉芳) | |
| dc.contributor.author | Bo-Cheng Chen | en |
| dc.contributor.author | 陳柏誠 | zh_TW |
| dc.date.accessioned | 2021-06-08T04:03:59Z | - |
| dc.date.copyright | 2018-08-30 | |
| dc.date.issued | 2018 | |
| dc.date.submitted | 2018-08-01 | |
| dc.identifier.citation | 1. Nagi R, Sahu S, Rakesh N. Molecular and genetic aspects in the etiopathogenesis of ameloblastoma: An update. J Oral Maxillofac Pathol. 2016;20(3):497-504.
2. Larsson A, Almeren H. Ameloblastoma of the jaws. An analysis of a consecutive series of all cases reported to the Swedish Cancer Registry during 1958--1971. Acta Pathol Microbiol Scand A. 1978;86A(5):337-49. 3. Regezi JA, Kerr DA, Courtney RM. Odontogenic tumors: analysis of 706 cases. J Oral Surg. 1978;36(10):771-8. 4. Savithri V, Janardhanan M, Suresh R, Kumar RV. Desmoplastic ameloblastoma with osteoplasia: Review of literature with a case report. J Oral Maxillofac Pathol. 2013;17(2):298-301. 5. Rizzitelli A, Smoll NR, Chae MP, Rozen WM, Hunter-Smith DJ. Incidence and overall survival of malignant ameloblastoma. PLoS One. 2015;10(2):e0117789. 6. Pereira NB, Pereira KM, Coura BP, Diniz MG, de Castro WH, Gomes CC, et al. BRAFV600E mutation in the diagnosis of unicystic ameloblastoma. J Oral Pathol Med. 2016;45(10):780-5. 7. Garcia NG, Oliveira DT, Rodrigues MT. Unicystic Ameloblastoma with Mural Proliferation Managed by Conservative Treatment. Case Rep Pathol. 2016;2016:3089540. 8. McClary AC, West RB, McClary AC, Pollack JR, Fischbein NJ, Holsinger CF, et al. Ameloblastoma: a clinical review and trends in management. Eur Arch Otorhinolaryngol. 2016;273(7):1649-61. 9. Reichart PA, Philipsen HP, Sonner S. Ameloblastoma: biological profile of 3677 cases. Eur J Cancer B Oral Oncol. 1995;31B(2):86-99. 10. Becelli R, Carboni A, Cerulli G, Perugini M, Iannetti G. Mandibular ameloblastoma: analysis of surgical treatment carried out in 60 patients between 1977 and 1998. J Craniofac Surg. 2002;13(3):395-400; discussion 11. Olaitan AA, Adeola DS, Adekeye EO. Ameloblastoma: clinical features and management of 315 cases from Kaduna, Nigeria. J Craniomaxillofac Surg. 1993;21(8):351-5. 12. Tranchina MG, Amico P, Galia A, Emmanuele C, Saita V, Fraggetta F. Ameloblastoma of the sinonasal tract: report of a case with clinicopathologic considerations. Case Rep Pathol. 2012;2012:218156. 13. Rosenstein T, Pogrel MA, Smith RA, Regezi JA. Cystic ameloblastoma--behavior and treatment of 21 cases. J Oral Maxillofac Surg. 2001;59(11):1311-6; discussion 6-8. 14. Curi MM, Dib LL, Pinto DS. Management of solid ameloblastoma of the jaws with liquid nitrogen spray cryosurgery. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997;84(4):339-44. 15. Muller H, Slootweg PJ. The ameloblastoma, the controversial approach to therapy. J Maxillofac Surg. 1985;13(2):79-84. 16. Ueno S, Mushimoto K, Shirasu R. Prognostic evaluation of ameloblastoma based on histologic and radiographic typing. J Oral Maxillofac Surg. 1989;47(1):11-5. 17. Pogrel MA. The use of liquid nitrogen cryotherapy in the management of locally aggressive bone lesions. J Oral Maxillofac Surg. 1993;51(3):269-73; discussion 74. 18. Huffman GG, Thatcher JW. Ameloblastoma--the conservative surgical approach to treatment: report of four cases. J Oral Surg. 1974;32(11):850-4. 19. Carlson ER, Marx RE. The ameloblastoma: primary, curative surgical management. J Oral Maxillofac Surg. 2006;64(3):484-94. 20. Vayvada H, Mola F, Menderes A, Yilmaz M. Surgical management of ameloblastoma in the mandible: Segmental mandibulectomy and immediate reconstruction with free fibula or deep circumflex iliac artery flap (evaluation of the long-term esthetic and functional results). J Oral Maxillofac Surg. 2006;64(10):1532-9. 21. Ndukwe KC, Adebiyi EK, Ugboko VI, Adeyemo WL, Ajayi FO, Ladeinde AL, et al. Ameloblastic carcinoma: a multicenter Nigerian study. J Oral Maxillofac Surg. 2010;68(9):2111-4. 22. Sehdev MK, Huvos AG, Strong EW, Gerold FP, Willis GW. Proceedings: Ameloblastoma of maxilla and mandible. Cancer. 1974;33(2):324-33. 23. Shatkin S, Hoffmeister FS. Ameloblastoma: a rational approach to therapy. Oral Surg Oral Med Oral Pathol. 1965;20(4):421-35. 24. Miyamoto CT, Brady LW, Markoe A, Salinger D. Ameloblastoma of the jaw. Treatment with radiation therapy and a case report. Am J Clin Oncol. 1991;14(3):225-30. 25. Ueda M, Kaneda T. Combined chemotherapy and radiotherapy for advanced maxillary ameloblastoma. A case report. J Craniomaxillofac Surg. 1991;19(6):272-4. 26. Kennedy WR, Werning JW, Kaye FJ, Mendenhall WM. Treatment of ameloblastoma and ameloblastic carcinoma with radiotherapy. Eur Arch Otorhinolaryngol. 2016;273(10):3293-7. 27. Ramadas K, Jose CC, Subhashini J, Chandi SM, Viswanathan FR. Pulmonary metastases from ameloblastoma of the mandible treated with cisplatin, adriamycin, and cyclophosphamide. Cancer. 1990;66(7):1475-9. 28. Grunwald V, Le Blanc S, Karstens JH, Weihkopf T, Kuske M, Ganser A, et al. Metastatic malignant ameloblastoma responding to chemotherapy with paclitaxel and carboplatin. Ann Oncol. 2001;12(10):1489-91. 29. Campbell D, Jeffrey RR, Wallis F, Hulks G, Kerr KM. Metastatic pulmonary ameloblastoma. An unusual case. Br J Oral Maxillofac Surg. 2003;41(3):194-6. 30. Amzerin M, Fadoukhair Z, Belbaraka R, Iraqui M, Boutayeb S, M'Rabti H, et al. Metastatic ameloblastoma responding to combination chemotherapy: case report and review of the literature. J Med Case Rep. 2011;5:491. 31. Heikinheimo K, Kurppa KJ, Laiho A, Peltonen S, Berdal A, Bouattour A, et al. Early dental epithelial transcription factors distinguish ameloblastoma from keratocystic odontogenic tumor. J Dent Res. 2015;94(1):101-11. 32. So F, Daley TD, Jackson L, Wysocki GP. Immunohistochemical localization of fibroblast growth factors FGF-1 and FGF-2, and receptors FGFR2 and FGFR3 in the epithelium of human odontogenic cysts and tumors. J Oral Pathol Med. 2001;30(7):428-33. 33. Myoken Y, Myoken Y, Okamoto T, Sato JD, Takada K. Immunohistochemical localization of fibroblast growth factor-1 (FGF-1) and FGF-2 in cultured human ameloblastoma epithelial cells and ameloblastoma tissues. J Oral Pathol Med. 1995;24(9):387-92. 34. Nakao Y, Mitsuyasu T, Kawano S, Nakamura N, Kanda S, Nakamura S. Fibroblast growth factors 7 and 10 are involved in ameloblastoma proliferation via the mitogen-activated protein kinase pathway. Int J Oncol. 2013;43(5):1377-84. 35. Kurppa KJ, Caton J, Morgan PR, Ristimaki A, Ruhin B, Kellokoski J, et al. High frequency of BRAF V600E mutations in ameloblastoma. J Pathol. 2014;232(5):492-8. 36. Holderfield M, Deuker MM, McCormick F, McMahon M. Targeting RAF kinases for cancer therapy: BRAF-mutated melanoma and beyond. Nat Rev Cancer. 2014;14(7):455-67. 37. Brown NA, Rolland D, McHugh JB, Weigelin HC, Zhao L, Lim MS, et al. Activating FGFR2-RAS-BRAF mutations in ameloblastoma. Clin Cancer Res. 2014;20(21):5517-26. 38. Sweeney RT, McClary AC, Myers BR, Biscocho J, Neahring L, Kwei KA, et al. Identification of recurrent SMO and BRAF mutations in ameloblastomas. Nat Genet. 2014;46(7):722-5. 39. Diniz MG, Gomes CC, Guimaraes BV, Castro WH, Lacerda JC, Cardoso SV, et al. Assessment of BRAFV600E and SMOF412E mutations in epithelial odontogenic tumours. Tumour Biol. 2015;36(7):5649-53. 40. Orton RJ, Sturm OE, Vyshemirsky V, Calder M, Gilbert DR, Kolch W. Computational modelling of the receptor-tyrosine-kinase-activated MAPK pathway. Biochem J. 2005;392(Pt 2):249-61. 41. Kolch W. Meaningful relationships: the regulation of the Ras/Raf/MEK/ERK pathway by protein interactions. Biochem J. 2000;351 Pt 2:289-305. 42. Bernards A. GAPs galore! A survey of putative Ras superfamily GTPase activating proteins in man and Drosophila. Biochim Biophys Acta. 2003;1603(2):47-82. 43. Davie JR, Spencer VA. Signal transduction pathways and the modification of chromatin structure. Prog Nucleic Acid Res Mol Biol. 2001;65:299-340. 44. Lum L, Beachy PA. The Hedgehog response network: sensors, switches, and routers. Science. 2004;304(5678):1755-9. 45. Rimkus TK, Carpenter RL, Qasem S, Chan M, Lo HW. Targeting the Sonic Hedgehog Signaling Pathway: Review of Smoothened and GLI Inhibitors. Cancers (Basel). 2016;8(2). 46. Brown NA, Betz BL. Ameloblastoma: A Review of Recent Molecular Pathogenetic Discoveries. Biomark Cancer. 2015;7(Suppl 2):19-24. 47. Baudino TA. Targeted Cancer Therapy: The Next Generation of Cancer Treatment. Curr Drug Discov Technol. 2015;12(1):3-20. 48. Kreppel M, Zoller J. Ameloblastoma-Clinical, radiological, and therapeutic findings. Oral Dis. 2018;24(1-2):63-6. 49. Almeida Rde A, Andrade ES, Barbalho JC, Vajgel A, Vasconcelos BC. Recurrence rate following treatment for primary multicystic ameloblastoma: systematic review and meta-analysis. Int J Oral Maxillofac Surg. 2016;45(3):359-67. 50. Onnis G, Palmieri G, Montesu MA, Satta R. Second primary melanoma on a patient undergoing vemurafenib therapy. A case report. Int J Dermatol. 2017;56(7):792-4. 51. Zhang W, Heinzmann D, Grippo JF. Clinical Pharmacokinetics of Vemurafenib. Clin Pharmacokinet. 2017;56(9):1033-43. 52. Hertzman Johansson C, Egyhazi Brage S. BRAF inhibitors in cancer therapy. Pharmacol Ther. 2014;142(2):176-82. 53. Gencler B, Gonul M. Cutaneous Side Effects of BRAF Inhibitors in Advanced Melanoma: Review of the Literature. Dermatol Res Pract. 2016;2016:5361569. 54. Doan HQ, Silapunt S, Migden MR. Sonidegib, a novel smoothened inhibitor for the treatment of advanced basal cell carcinoma. Onco Targets Ther. 2016;9:5671-8. 55. Heikinheimo K, Kurppa KJ, Elenius K. Novel targets for the treatment of ameloblastoma. J Dent Res. 2015;94(2):237-40. 56. Menzies AM, Long GV. Systemic treatment for BRAF-mutant melanoma: where do we go next? Lancet Oncol. 2014;15(9):e371-81. 57. Paraiso KH, Fedorenko IV, Cantini LP, Munko AC, Hall M, Sondak VK, et al. Recovery of phospho-ERK activity allows melanoma cells to escape from BRAF inhibitor therapy. Br J Cancer. 2010;102(12):1724-30. 58. Kim J, Aftab BT, Tang JY, Kim D, Lee AH, Rezaee M, et al. Itraconazole and arsenic trioxide inhibit Hedgehog pathway activation and tumor growth associated with acquired resistance to smoothened antagonists. Cancer Cell. 2013;23(1):23-34. 59. Kaye FJ, Ivey AM, Drane WE, Mendenhall WM, Allan RW. Clinical and radiographic response with combined BRAF-targeted therapy in stage 4 ameloblastoma. J Natl Cancer Inst. 2015;107(1):378. 60. Tan S, Pollack JR, Kaplan MJ, Colevas AD, West RB. BRAF inhibitor treatment of primary BRAF-mutant ameloblastoma with pathologic assessment of response. Oral Surg Oral Med Oral Pathol Oral Radiol. 2016;122(1):e5-7. 61. Faden DL, Algazi A. Durable treatment of ameloblastoma with single agent BRAFi Re: Clinical and radiographic response with combined BRAF-targeted therapy in stage 4 ameloblastoma. J Natl Cancer Inst. 2017;109(1). 62. Marshall CJ. MAP kinase kinase kinase, MAP kinase kinase and MAP kinase. Curr Opin Genet Dev. 1994;4(1):82-9. 63. Moodie SA, Wolfman A. The 3Rs of life: Ras, Raf and growth regulation. Trends Genet. 1994;10(2):44-8. 64. Morrison DK, Cutler RE. The complexity of Raf-1 regulation. Curr Opin Cell Biol. 1997;9(2):174-9. 65. Cutler RE, Jr., Stephens RM, Saracino MR, Morrison DK. Autoregulation of the Raf-1 serine/threonine kinase. Proc Natl Acad Sci U S A. 1998;95(16):9214-9. 66. Bonner TI, Oppermann H, Seeburg P, Kerby SB, Gunnell MA, Young AC, et al. The complete coding sequence of the human raf oncogene and the corresponding structure of the c-raf-1 gene. Nucleic Acids Res. 1986;14(2):1009-15. 67. Beck TW, Huleihel M, Gunnell M, Bonner TI, Rapp UR. The complete coding sequence of the human A-raf-1 oncogene and transforming activity of a human A-raf carrying retrovirus. Nucleic Acids Res. 1987;15(2):595-609. 68. Fukui M, Yamamoto T, Kawai S, Maruo K, Toyoshima K. Detection of a raf-related and two other transforming DNA sequences in human tumors maintained in nude mice. Proc Natl Acad Sci U S A. 1985;82(17):5954-8. 69. Stanton VP, Jr., Cooper GM. Activation of human raf transforming genes by deletion of normal amino-terminal coding sequences. Mol Cell Biol. 1987;7(3):1171-9. 70. Cantwell-Dorris ER, O'Leary JJ, Sheils OM. BRAFV600E: implications for carcinogenesis and molecular therapy. Mol Cancer Ther. 2011;10(3):385-94. 71. Rubinstein JC, Sznol M, Pavlick AC, Ariyan S, Cheng E, Bacchiocchi A, et al. Incidence of the V600K mutation among melanoma patients with BRAF mutations, and potential therapeutic response to the specific BRAF inhibitor PLX4032. J Transl Med. 2010;8:67. 72. Pakneshan S, Salajegheh A, Smith RA, Lam AK. Clinicopathological relevance of BRAF mutations in human cancer. Pathology. 2013;45(4):346-56. 73. Falini B, Martelli MP, Tiacci E. BRAF V600E mutation in hairy cell leukemia: from bench to bedside. Blood. 2016;128(15):1918-27. 74. Haroche J, Charlotte F, Arnaud L, von Deimling A, Helias-Rodzewicz Z, Hervier B, et al. High prevalence of BRAF V600E mutations in Erdheim-Chester disease but not in other non-Langerhans cell histiocytoses. Blood. 2012;120(13):2700-3. 75. Manfredi L, Meyer N, Tournier E, Grand D, Uro-Coste E, Rochaix P, et al. Highly Concordant Results Between Immunohistochemistry and Molecular Testing of Mutated V600E BRAF in Primary and Metastatic Melanoma. Acta Derm Venereol. 2016;96(5):630-4. 76. Sun J, Zhang J, Lu J, Gao J, Lu T, Ren X, et al. Immunohistochemistry is highly sensitive and specific for detecting the BRAF V600E mutation in papillary thyroid carcinoma. Int J Clin Exp Pathol. 2015;8(11):15072-8. 77. Yao Z, Yaeger R, Rodrik-Outmezguine VS, Tao A, Torres NM, Chang MT, et al. Tumours with class 3 BRAF mutants are sensitive to the inhibition of activated RAS. Nature. 2017;548(7666):234-8. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/22128 | - |
| dc.description.abstract | 造釉細胞瘤是一種常見的齒源性上皮腫瘤，主要好發在顎骨，此腫瘤雖然在定義上為良性，但卻相當具有侵襲性，並且容易復發，而目前標準治療造釉細胞瘤的方法是廣泛性大範圍切除且合併顎骨切除，而造成臉部顏面功能的損傷且影響美觀甚劇，然而在近年來對於造釉細胞瘤之致病機轉有了突破性的發現，有超過八成的造釉細胞瘤的病人都有MAPK (FGFR-RAS-RAF) pathway上的突變，而其中的BRAF(V600E)的突變占了其中的六成，顯示BRAF(V600E)可能是造成造釉細胞瘤的關鍵基因，此外在Sonic hedgehog pathway (SHH) 裡的SMO基因則是被發現有近四成的基因突變，在不同突變上的造釉細胞瘤也會造就不同病理形態上的差別。而在黑色素細胞瘤和大腸直腸癌中都有利用MAPK pathway和Sonic hedgehog pathway相關的標靶藥物的治療案例，而在先前的文獻中也有提到三位造釉細胞瘤患者，使用了MAPK pathway的小分子標靶藥物治療而讓腫瘤縮小的案例，這顯示了標靶藥物可能在未來是可以成為取代手術性切除的治療方式。
我們的研究致力於找出MAPK pathway中的BRAF(V600E)突變在造釉細胞瘤中所扮演著角色，分別在齒源性上皮細胞中送入了GFP和BRAF(V600E)的基因，模擬正常齒源性細胞在受到致癌基因的調控下所產生的變化，並針對其致癌基因所調控的基因去做一系列研究，結果發現在具有BRAF(V600E)表現的齒源性上皮細胞呈現老化的細胞型態，並且在會跨越老化型態走向進入細胞週期中，且與幹細胞基因SOX2有非常巨大的相關；而在我們自己建立的老鼠模型中也發現了在具有BRAF(V600E)大量表現的齒源性上皮細胞能使老鼠產生腫瘤，這也顯示了BRAF(V600E)的確在造釉細胞瘤中的致病機轉中扮演著莫大的角色，若能清楚的了解BRAF(V600E)的致病機轉，相信以後在治療造釉細胞瘤中是一個莫大的突破。 | zh_TW |
| dc.description.abstract | Ameloblastoma is a benign and rare neoplasm and the most prevalent amongst epithelial odontogenic neoplasm. Because of its locally aggressive property and high recurrence rate, surgical resection is often required to treat the condition, which could lead to facial dysfunction and significant morbidity. Recent studies have reported frequent mutations in MAPK (FGFR-RAS-RAF) pathway and SMO in ameloblastoma, among which BRAF(V600E) mutations is most commonly found. Since MAPK pathway and SMO mutations have also been identified in other cancers such as malignant melanoma and colorectal cancer, targeted therapy for treating those cancers by targeting these mutations. In addition, there have been three case reports suggesting the success of BRAF and MEK inhibitors in treating BRAF mediated ameloblastoma patients.
In order to establish targeted therapy in the future, the aim of our study is to investigate the role of BRAF(V600E) mutations in the pathogenesis of ameloblastoma. We transfected GFP and BRAF(V600E) individually into odential epithelial cells- HERS (Hertwig's epithelial cells) to mimic series of situations for the normal odential epithelial cells effected by the oncogene BRAF(V600E). We discovered that the BRAF(V600E) infected HERS takes on a cellular senescence look in the cellular morphology and overcomes the senescence status in cellular cycle at the late stage. The phenomenon of senescence is thought to have direct relation with stemness gene, SOX2. We established the ameloblastoma mouse model and showed that BRAF(V600E) harboring but not GFP only HERS could initiate tumorigenesis on the back of nude mice. This result showed that BRAF(V600E) has a great impact on the pathogenesis of ameloblastoma. Better understanding of the pathogenesis cascade of BRAF(V600) could have significant impact on developing the treatment for ameloblastoma. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-08T04:03:59Z (GMT). No. of bitstreams: 1 ntu-107-R05450001-1.pdf: 2969949 bytes, checksum: a1c7d8cf54d222774fc73d0c12fccdf0 (MD5) Previous issue date: 2018 | en |
| dc.description.tableofcontents | 誌謝 2
中文摘要 3 ABSTRACT 4 CONTENTS 6 Introduction 8 Epidemiology of ameloblastoma 8 Introduction of ameloblastoma 9 Clinical radiographic features of ameloblastoma 12 Treatment of ameloblastoma 13 Surgery 13 Radiotherapy and chemotherapy 16 Molecular biology and pathogenesis of ameloblastoma 16 Genetic background of ameloblastoma 16 Mitogen activated protein kinase (MAPK)/ extracellular signal-regulated kinase (ERK) pathway 20 Sonic hedgehog (Shh) pathway 22 Clinicopathologic associations of mutational profiles in ameloblastoma 23 The potentiality of targeted treatment for ameloblastoma 24 Introduction of targeted therapy 24 Potentially targeted therapy for ameloblastoma 26 BRAF inhibitors 27 MEK inhibitors 28 Target Hedgehog pathway inhibitors 29 Drug resistance 29 Clinical reports of targeted therapy for ameloblastoma patients 31 Introduction to BRAF protein and BRAF (V600E) mutation 33 BRAF protein 33 BRAF(V600E) mutation 34 Materials and methods 36 Cell lines and culture condition 36 Plasmids and lentivirus preparation 36 Western blot analysis 37 RNA extraction and purification 39 Reverse transcription PCR 39 Quantitative reverse transcription polymerase chain reaction (qRT-PCR) 40 Immunohistochemistry 40 Flow cytometry for cell cycle analysis 41 Senescence β-galactosidase Staining 42 Statistical analysis 42 Results 43 BRAF(V600E) in HERS cells impairs cell viability 43 BRAF(V600E) in HERS cells causes senescence 43 BRAF(V600E) in HERS cells enhances the expression of cell cycle regulators 44 BRAF(V600E) in HERS cells promotes cells migration 45 BRAF(V600E) in HERS cells induces tumor growth in xenograft mouse model 45 Inhibition of BRAF(V600E) pathway causes ameloblastoma cell lines death 46 Suppression of SOX2 in ameloblastoma cell lines causes downregulation in cell viability. 47 BRAF/MAPK inhibition induces resistant clones of ameloblastoma and upregulates stemness marker SOX2 in AM-1 48 BRAF(V600E) in HERS cells induce the krt3, krt17, kr19 and gli1 mRNA expression. 49 Discussion 50 Table 53 Figures 54 Conclusions 68 References 69 | |
| dc.language.iso | en | |
| dc.subject | 標靶治療 | zh_TW |
| dc.subject | SOX2 | zh_TW |
| dc.subject | 造釉細胞瘤 | zh_TW |
| dc.subject | BRAF(V600E) | zh_TW |
| dc.subject | ameloblastoma | en |
| dc.subject | SOX2 | en |
| dc.subject | BRAF(V600E) | en |
| dc.subject | targeted therapy | en |
| dc.title | BRAF(V600E)突變在造釉細胞瘤中所扮演的致病機轉 | zh_TW |
| dc.title | The role of BRAF(V600E) mutation in the pathogenesis of ameloblastoma | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 106-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 吳漢忠(Han-Chung Wu 吳漢忠),沈家寧(Shen, Chia-Ning 沈家寧) | |
| dc.subject.keyword | 造釉細胞瘤,BRAF(V600E),標靶治療,SOX2, | zh_TW |
| dc.subject.keyword | ameloblastoma,BRAF(V600E),targeted therapy,SOX2, | en |
| dc.relation.page | 76 | |
| dc.identifier.doi | 10.6342/NTU201802233 | |
| dc.rights.note | 未授權 | |
| dc.date.accepted | 2018-08-01 | |
| dc.contributor.author-college | 醫學院 | 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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