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      Diffuse Large B Cell Lymphoma Shows Distinct MethylationProfiles of the Tumor Suppressor Genes among theNon-Hodgkin’s Lymphomas

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      https://www.riss.kr/link?id=A101633363

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      다국어 초록 (Multilingual Abstract)

      Aberrant methylation of CpG islands in promoter regions is one of the major
      mechanisms for silencing of tumor suppressor genes in various types of human cancers including
      non-Hodgkin’s lymphomas (NHL). In this study, we investigated the aberrant promoter
      methylation status of known or suspected tumor suppressor genes in NHLs and compared
      the methylation profiles between B-cell and T/NK-cell NHLs. Methods : 54 cases of B-cell NHLs
      and 16 cases of T/NK-cell NHLs were examined for the methylation status of eight genes
      using methylation specific PCR. Results : CpG islands methylation was variously found in
      eight genes as follows; DAPK (71%), MT1G (70%), p16 (53%), CDH1 (53%), THBS1 (56%),
      MGMT (27.1%), COX2 (13%), and RUNX3 (11.4%). In six cases (8 %), methylation was not
      observed in any of these genes. Overall methylation index of B-cell NHLs (0.48) was significantly
      higher than that of T/NK-cell NHLs (0.32). Of eight genes tested, THBS1 and CDH1
      methylations were much more prominent in diffuse large B-cell lymphomas than in T/NK-cell
      NHLs or other B-cell NHLs. Conclusion : This study suggests that aberrant CpG island methylation
      is a frequent event in NHLs, and diffuse large B-cell lymphomas show overlapping but
      distinct methylation profiles.
      번역하기

      Aberrant methylation of CpG islands in promoter regions is one of the major mechanisms for silencing of tumor suppressor genes in various types of human cancers including non-Hodgkin’s lymphomas (NHL). In this study, we investigated the aberrant pro...

      Aberrant methylation of CpG islands in promoter regions is one of the major
      mechanisms for silencing of tumor suppressor genes in various types of human cancers including
      non-Hodgkin’s lymphomas (NHL). In this study, we investigated the aberrant promoter
      methylation status of known or suspected tumor suppressor genes in NHLs and compared
      the methylation profiles between B-cell and T/NK-cell NHLs. Methods : 54 cases of B-cell NHLs
      and 16 cases of T/NK-cell NHLs were examined for the methylation status of eight genes
      using methylation specific PCR. Results : CpG islands methylation was variously found in
      eight genes as follows; DAPK (71%), MT1G (70%), p16 (53%), CDH1 (53%), THBS1 (56%),
      MGMT (27.1%), COX2 (13%), and RUNX3 (11.4%). In six cases (8 %), methylation was not
      observed in any of these genes. Overall methylation index of B-cell NHLs (0.48) was significantly
      higher than that of T/NK-cell NHLs (0.32). Of eight genes tested, THBS1 and CDH1
      methylations were much more prominent in diffuse large B-cell lymphomas than in T/NK-cell
      NHLs or other B-cell NHLs. Conclusion : This study suggests that aberrant CpG island methylation
      is a frequent event in NHLs, and diffuse large B-cell lymphomas show overlapping but
      distinct methylation profiles.

      더보기

      다국어 초록 (Multilingual Abstract)

      Aberrant methylation of CpG islands in promoter regions is one of the major
      mechanisms for silencing of tumor suppressor genes in various types of human cancers including
      non-Hodgkin’s lymphomas (NHL). In this study, we investigated the aberrant promoter
      methylation status of known or suspected tumor suppressor genes in NHLs and compared
      the methylation profiles between B-cell and T/NK-cell NHLs. Methods : 54 cases of B-cell NHLs
      and 16 cases of T/NK-cell NHLs were examined for the methylation status of eight genes
      using methylation specific PCR. Results : CpG islands methylation was variously found in
      eight genes as follows; DAPK (71%), MT1G (70%), p16 (53%), CDH1 (53%), THBS1 (56%),
      MGMT (27.1%), COX2 (13%), and RUNX3 (11.4%). In six cases (8 %), methylation was not
      observed in any of these genes. Overall methylation index of B-cell NHLs (0.48) was significantly
      higher than that of T/NK-cell NHLs (0.32). Of eight genes tested, THBS1 and CDH1
      methylations were much more prominent in diffuse large B-cell lymphomas than in T/NK-cell
      NHLs or other B-cell NHLs. Conclusion : This study suggests that aberrant CpG island methylation
      is a frequent event in NHLs, and diffuse large B-cell lymphomas show overlapping but
      distinct methylation profiles.
      번역하기

      Aberrant methylation of CpG islands in promoter regions is one of the major mechanisms for silencing of tumor suppressor genes in various types of human cancers including non-Hodgkin’s lymphomas (NHL). In this study, we investigated the aberrant p...

      Aberrant methylation of CpG islands in promoter regions is one of the major
      mechanisms for silencing of tumor suppressor genes in various types of human cancers including
      non-Hodgkin’s lymphomas (NHL). In this study, we investigated the aberrant promoter
      methylation status of known or suspected tumor suppressor genes in NHLs and compared
      the methylation profiles between B-cell and T/NK-cell NHLs. Methods : 54 cases of B-cell NHLs
      and 16 cases of T/NK-cell NHLs were examined for the methylation status of eight genes
      using methylation specific PCR. Results : CpG islands methylation was variously found in
      eight genes as follows; DAPK (71%), MT1G (70%), p16 (53%), CDH1 (53%), THBS1 (56%),
      MGMT (27.1%), COX2 (13%), and RUNX3 (11.4%). In six cases (8 %), methylation was not
      observed in any of these genes. Overall methylation index of B-cell NHLs (0.48) was significantly
      higher than that of T/NK-cell NHLs (0.32). Of eight genes tested, THBS1 and CDH1
      methylations were much more prominent in diffuse large B-cell lymphomas than in T/NK-cell
      NHLs or other B-cell NHLs. Conclusion : This study suggests that aberrant CpG island methylation
      is a frequent event in NHLs, and diffuse large B-cell lymphomas show overlapping but
      distinct methylation profiles.

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      참고문헌 (Reference)

      1 Roth MJ, "p16, MGMT, RARbeta2, CLDN3, CRBP and MT1G gene methylation in esophageal squamous cell carcinoma and its precursor lesions" 15 : 1591-1597, 2006

      2 Jones PA, "The fundamental role of epigenetic events in cancer" 3 : 415-428, 2002

      3 Akhtar M, "Promoter methylation regulates Helicobacter pylori-stimulated cyclooxygenase-2 expression in gastric epithelial cells" 61 : 2399-2403, 2001

      4 Jaffe ES, "Oxford University Press [distributor]" 351-, 2001

      5 Morris MR, "Multigene methylation analysis of Wilms’ tumour and adult renal cell carcinoma" 22 : 6794-6801, 2003

      6 Herman JG, "Methylation- specific PCR: a novel PCR assay for methylation status of CpG islands" 93 : 9821-9826, 1996

      7 Li Q, "Methylation and silencing of the Thrombospondin-1 promoter in human cancer" 18 : 3284-3289, 1999

      8 Henrique R, "MT1G hypermethylation is associated with higher tumor stage in prostate cancer" 14 : 1274-1278, 2005

      9 Huang Y, "Hypermethylation, but not LOH, is associated with the low expression of MT1G and CRABP1 in papillary thyroid carcinoma" 104 : 735-744, 2003

      10 Esteller M, "Hypermethylation of the DNA repair gene O(6)-methylguanine DNA methyltransferase and survival of patients with diffuse large B-cell lymphoma" 94 : 26-32, 2002

      1 Roth MJ, "p16, MGMT, RARbeta2, CLDN3, CRBP and MT1G gene methylation in esophageal squamous cell carcinoma and its precursor lesions" 15 : 1591-1597, 2006

      2 Jones PA, "The fundamental role of epigenetic events in cancer" 3 : 415-428, 2002

      3 Akhtar M, "Promoter methylation regulates Helicobacter pylori-stimulated cyclooxygenase-2 expression in gastric epithelial cells" 61 : 2399-2403, 2001

      4 Jaffe ES, "Oxford University Press [distributor]" 351-, 2001

      5 Morris MR, "Multigene methylation analysis of Wilms’ tumour and adult renal cell carcinoma" 22 : 6794-6801, 2003

      6 Herman JG, "Methylation- specific PCR: a novel PCR assay for methylation status of CpG islands" 93 : 9821-9826, 1996

      7 Li Q, "Methylation and silencing of the Thrombospondin-1 promoter in human cancer" 18 : 3284-3289, 1999

      8 Henrique R, "MT1G hypermethylation is associated with higher tumor stage in prostate cancer" 14 : 1274-1278, 2005

      9 Huang Y, "Hypermethylation, but not LOH, is associated with the low expression of MT1G and CRABP1 in papillary thyroid carcinoma" 104 : 735-744, 2003

      10 Esteller M, "Hypermethylation of the DNA repair gene O(6)-methylguanine DNA methyltransferase and survival of patients with diffuse large B-cell lymphoma" 94 : 26-32, 2002

      11 Katzenellenbogen RA, "Hypermethylation of the DAP-kinase CpG island is a common alteration in B-cell malignancies" 93 : 4347-4353, 1999

      12 Ueki T, "Hypermethylation of multiple genes in pancreatic adenocarcinoma" 60 : 1835-1839, 2000

      13 Baur AS, "Frequent methylation silencing of p15(INK4b) (MTS2) and p16 (INK4a) (MTS1) in B-cell and T-cell lymphomas" 94 : 1773-1781, 1999

      14 Chu LC, "Epigenetic silencing of multiple genes in primary CNS lymphoma" 119 : 2487-2491, 2006

      15 Takahashi T, "DNA methylation profiles of lymphoid and hematopoietic malignancies" 10 : 2928-2935, 2004

      16 Esteller M, "CpG island hypermethylation and tumor suppressor genes: a booming present, a brighter future" 21 : 5427-5440, 2002

      17 Santini V, "Changes in DNA methylation in neoplasia: pathophysiology and therapeutic implications" 134 : 573-586, 2001

      18 Li QL, "Causal relationship between the loss of RUNX3 expression and gastric cancer" 109 : 113-124, 2002

      19 Maruyama R, "Aberrant promoter methylation profile of bladder cancer and its relationship to clinicopathological features" 61 : 8659-8663, 2001

      20 Rossi D, "Aberrant promoter methylation of multiple genes throughout the clinico-pathologic spectrum of B-cell neoplasia" 89 : 154-164, 2004

      21 Toyota M, "Aberrant methylation of the Cyclooxygenase 2 CpG island in colorectal tumors" 60 : 4044-4048, 2000

      22 Costello JF, "Aberrant CpG-island methylation has non-random and tumour-type-specific patterns" 24 : 132-138, 2000

      23 Kang GH, "Aberrant CpG island hypermethylation of multiple genes in prostate cancer and prostatic intraepithelial neoplasia" 202 : 233-240, 2004

      24 Esteller M, "A gene hypermethylation profile of human cancer" 61 : 3225-3229, 2001

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      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2023 평가예정 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
      2020-01-01 평가 등재학술지 유지 (해외등재 학술지 평가) KCI등재
      2014-12-24 학술지명변경 한글명 : The Korean Journal of Pathology -> Journal of Pathology and Translational Medicine
      외국어명 : The Korean Journal of Pathology -> Journal of Pathology and Translational Medicine
      KCI등재
      2010-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2009-04-13 학술지명변경 한글명 : 대한병리학회지 -> The Korean Journal of Pathology KCI등재
      2007-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2005-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2002-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      1999-07-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
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      학술지 인용정보

      학술지 인용정보
      기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
      2016 0.13 0.13 0.12
      KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
      0.13 0.11 0.409 0.01
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