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      KCI등재후보

      구강 편평세포암종과 법랑아세포종에서 Fas, Fas-L, FAP-1 발현에 관한 면역 병리학적 연구

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      https://www.riss.kr/link?id=A103107936

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      다국어 초록 (Multilingual Abstract)

      The purpose of this study was to evaluate the role of Fas, Fas-L, and FAP-1 expression in the oral squamous cell carcinomas and ameloblastomas. For this study, 10 subjects diagnosed as squamous cell carcinoma and 8 subjects of ameloblastoma referred to the Dept. of Oral Pathology, School of Dentistry, Kyung Hee University, 5 subjects of normal oral mucosa without any inflammatory changes were used as experimental, control groups respectively. All the tissues ; experimental and control group were fixed in neutral formalin solution and embedded in paraffin, serial tissue section were made 5㎛ in thickness and processed in the standard way for immunohistochemical method, using primary antibody against Fas, Fas-L, FAP-1, each was diluted at 1;100 followed by the super sensitive non- biotin horse radish peroxidase detection system with DAB as chormogen, counterstained with Gill's hematoxylin stain method , mounted. And examined under the biologic microscope with the criteria of -(no epithelial stain), +(weak or focal epithelial stain), ++(moderate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelial, and connective tissue component in squamous cell carcinomas , ameloblastomas and normal oral mucosa on each. In normal oral epithelium, negative reaction was noted on the Fas . Fas-L stain, but on FAP-1 reaction, tumors cells with intense reaction on nuclei and cytoplasm or negative reaction on nuclei with intense reaction on cytoplasm were admixed. On Fas, Fas-1 reaction, both tumor cells of ameloblastoma and oral squamous cell carcinoma showed negative reaction on nuclei and cytoplasms. On FAP-1 reaction, tumor cells of oral squamous cell carcinomas showed more intensive response compare to that on ameloblastomas. Considering these results, the tumor cells of ameloblastoma and squamous cell carcinoma showed negative reaction on the Fas and Fas-L, but it could suggest that FAP-1 induce the development of tumors by means of inhibition of the apoptosis.
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      The purpose of this study was to evaluate the role of Fas, Fas-L, and FAP-1 expression in the oral squamous cell carcinomas and ameloblastomas. For this study, 10 subjects diagnosed as squamous cell carcinoma and 8 subjects of ameloblastoma referred t...

      The purpose of this study was to evaluate the role of Fas, Fas-L, and FAP-1 expression in the oral squamous cell carcinomas and ameloblastomas. For this study, 10 subjects diagnosed as squamous cell carcinoma and 8 subjects of ameloblastoma referred to the Dept. of Oral Pathology, School of Dentistry, Kyung Hee University, 5 subjects of normal oral mucosa without any inflammatory changes were used as experimental, control groups respectively. All the tissues ; experimental and control group were fixed in neutral formalin solution and embedded in paraffin, serial tissue section were made 5㎛ in thickness and processed in the standard way for immunohistochemical method, using primary antibody against Fas, Fas-L, FAP-1, each was diluted at 1;100 followed by the super sensitive non- biotin horse radish peroxidase detection system with DAB as chormogen, counterstained with Gill's hematoxylin stain method , mounted. And examined under the biologic microscope with the criteria of -(no epithelial stain), +(weak or focal epithelial stain), ++(moderate or focal intensive epithelial stain), +++(intense generalized epithelial staining) for the epithelial, and connective tissue component in squamous cell carcinomas , ameloblastomas and normal oral mucosa on each. In normal oral epithelium, negative reaction was noted on the Fas . Fas-L stain, but on FAP-1 reaction, tumors cells with intense reaction on nuclei and cytoplasm or negative reaction on nuclei with intense reaction on cytoplasm were admixed. On Fas, Fas-1 reaction, both tumor cells of ameloblastoma and oral squamous cell carcinoma showed negative reaction on nuclei and cytoplasms. On FAP-1 reaction, tumor cells of oral squamous cell carcinomas showed more intensive response compare to that on ameloblastomas. Considering these results, the tumor cells of ameloblastoma and squamous cell carcinoma showed negative reaction on the Fas and Fas-L, but it could suggest that FAP-1 induce the development of tumors by means of inhibition of the apoptosis.

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      참고문헌 (Reference)

      1 Nagata S, "he Fas death factor." 267 : 1449-1456, 1995

      2 Chen Q, "Up-regulation of Fas ligand and down-regulation of Fas expression in oral carcinogenesis." 35 : 548-553, 1999

      3 Itoh N, "The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis." 66 : 233-43, 1991

      4 Itoh N, "The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis" 66 : 233-343, 1991

      5 Vaux D.L, "The molelcular biology of apoptosis" 93 : 2239-2244, 1996

      6 Wang X, "The expression of Fas and bcl-2 in hamster buccal carcinogenesis." 14 (14): 155-158, 2005

      7 Watanabe-Fukunaga R, "The cDNA sructure ,expression and chromosomal assignmnet of the mouse Fas antigen." 148 : 1274-1279, 1992

      8 Somma P, "Squamous cell carcinoma of the lower lip: FAS/FASL expression, lymphocyte subtypes and outcome." 18 (18): 59-64, 2005

      9 McCall C.A, "Programmed cell death in terminally differentiating keratinocytes: role of endogenous endonuclease." 97 : 111-114, 2001

      10 Jacobson M.D, "Programmed cell death in animal development." 88 : 347-354, 1997

      1 Nagata S, "he Fas death factor." 267 : 1449-1456, 1995

      2 Chen Q, "Up-regulation of Fas ligand and down-regulation of Fas expression in oral carcinogenesis." 35 : 548-553, 1999

      3 Itoh N, "The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis." 66 : 233-43, 1991

      4 Itoh N, "The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis" 66 : 233-343, 1991

      5 Vaux D.L, "The molelcular biology of apoptosis" 93 : 2239-2244, 1996

      6 Wang X, "The expression of Fas and bcl-2 in hamster buccal carcinogenesis." 14 (14): 155-158, 2005

      7 Watanabe-Fukunaga R, "The cDNA sructure ,expression and chromosomal assignmnet of the mouse Fas antigen." 148 : 1274-1279, 1992

      8 Somma P, "Squamous cell carcinoma of the lower lip: FAS/FASL expression, lymphocyte subtypes and outcome." 18 (18): 59-64, 2005

      9 McCall C.A, "Programmed cell death in terminally differentiating keratinocytes: role of endogenous endonuclease." 97 : 111-114, 2001

      10 Jacobson M.D, "Programmed cell death in animal development." 88 : 347-354, 1997

      11 Holbaum A.M, "Opposing effects of transmembrane and soluble Fas ligand expression on inflammation and tumor cell survival." 191 : 1209-1219, 2000

      12 Suda T, "Molecular cloning and expression of the Fas ligand , a novel member of the tumor necrosis factor family." 75 : 1169-1178, 1993

      13 Arends M, "Mechanisms and roles in pathology" 32 : 223-254, 2001

      14 Steller H, "Mechanisms and genes of cellular suicide." 267 : 1445-1449, 1995

      15 Ellis R.E, "Mechanisms and findings of cell death." 7 : 663-698, 1991

      16 Hake A.R.,Polakowska R.R, "J Invest Dermatol" 101 : 107-112, 1993

      17 Chun K.H, "Induction of apoptosis by the synthetic retinoid MX3350-1 through extrinsic and intrinsic pathways in head and neck squamous carcinoma cells." 24 (24): 3669-3677, 2005

      18 Kaufmann. S.T, "Induction of apoptosis by cancer chemotherapy." 256 : 42-29, 2000

      19 Murakami Y, "Immunohistochemical detection of Fas antigen in oral epithelia." 26 : 57-62, 1997

      20 Yoshioka C, "Identification of the Fas amtogen in human gingival." 75 : 1353-1357, 1996

      21 Wyllie A.H, "Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation." 284 : 555-556, 1980

      22 Kim J.W, "Fas ligand-positive membranous vesicles isolated from sera of patients with oral cancer induce apoptosis of activated T lymphocytes." 11 (11): 1010-1020, 2005

      23 Griffith T.S, "Fas ligand-induced apoptosis as a mechanism of immune privilege." 270 : 1189-1192, 1995

      24 Gastman B.R, "Fas ligand is expressed on human squamous cell carcinomas of the head and neck, it promotes apoptosis of T lymphocytes." 59 : 5356-5364, 1999

      25 Seta C, "Fas expression and Fas monoclonal antibody-induced apoptosis in human squamous cell carcinoma cell line,SCC-25." 29 : 271-278, 2000

      26 Muraki Y, "Fas antigen expression and outcome of oral squamous cell carcinoma." 29 : 360-365, 2000

      27 Chinnaiyan A.M, "FADD, a novel death domoain-containing protein,interacts with the death domain of Fas and initiates apoptosis." 81 : 505-512, 2005

      28 Fujieda S, "Expression of Fas(CD95) ligand is correlated with IL-10 and granulocyte colony-stimulating factor expression in oral and oropharyngeal squamous cell carcinoma." 161 : 73-81, 2000

      29 Sayama K, "Expression of Fas antigen on keratinocytes in vivo and induction of apoptosis in cultured keratinocytes." 103 : 330-334, 1994

      30 Guler N, "Expression of Fas and Fas-ligand and analysis of argyrophilic nucleolar organizer regions in squamous cell carcinoma: relationships with tumor stage and grade, and apoptosis." 18 : 1-7, 2005

      31 Nariai Y, "Expression of FAP-1 in oral cancer cells In: Varma. A.K and Reade. P, Editors, Oral oncologyvol. 9" Macmillan India, New Dehli 209-218, 2003

      32 Dybikowska A, "Evaluation of Fas gene promoter polymorphism in cervical cancer patients." 14 (14): 475-478, 2004

      33 Mishima K, "Etodolac, a selective cyclo-oxygenase-2 inhibitor, enhances carboplatin-induced apoptosis of human tongue carcinoma cells by down-regulation of Fap-1 expression." 41 (41): 77-81, 2005

      34 Ravid Ramakas K, "De novo programmed cell death in oral cancer." 34 : 241-249, 1999

      35 Jackel M.C, "Clinical relevance of Fas(APO-1/CD95) expression in laryngeal squamous cell carcinoma." 23 : 646-652, 2001

      36 Schneider P, "Characterization of Fas(Apo-1, CD95)- Fas ligand interaction." 272 : 1997

      37 Mishima K, "Carboplatin induces Fas(APO-1/CD95)-dependent apoptosis of human tongue carcinoma cells: sensitization for apoptosis by uprequlation of FADD expression" 105 : 593-600, 2003

      38 Itakura M, "Both HPV and carcinogen contribute to the development of resistance to apoptosis during oral carcinogenesis." 16 (16): 591-597, 2000

      39 Reed J.C, "Bcl-2 and the regulation of programmed cell death" 124 : 1-6, 1994

      40 Kerr J.F.R, "Apoptosis: its significance in cancer and cancer therapy." 73 : 2013-2026, 1994

      41 Kerr J.F.R, "Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics." 26 : 239-257, 1972

      42 Mishima. K, "Apoptosis of human tongue carcinoma cells induced by anticancer drugs In: Varma. A.K and Reade. P, Editors, Oral oncologyvol. 9" Macmillan India, New Delhi 201-208, 2003

      43 Thompson C.B, "Apoptosis in the pathogenesis and treatment of disease." 267 : 1456-1462, 1995

      44 Yagita H, "Antitumor effect of locally produced CD95 ligand." 3 : 165-170, 1997

      45 Sato T, "A rpotein tyrosine phosphatase that associates with Fas/APO-1(CD95)" 268 : 411-415, 1995

      46 Itoh N, "A novel protein domain required for apoptosis. Mutational analysis of human Fas antigen, Biol." 268 : 1993

      47 Itoh N, "A novel protein domain required for apoptosis. Mutational analysis of human Fas antigen" 268 : 1993

      48 Busch C, "A grading system form the immunostaining of a A, B and H blood group isoantigens in bladder carcinoma." 8 : 81-88, 1988

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
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      2007-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2006-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.17 0.17 0.16
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.12 0.1 0.386 0
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