RISS 학술연구정보서비스

검색
다국어 입력

http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.

변환된 중국어를 복사하여 사용하시면 됩니다.

예시)
  • 中文 을 입력하시려면 zhongwen을 입력하시고 space를누르시면됩니다.
  • 北京 을 입력하시려면 beijing을 입력하시고 space를 누르시면 됩니다.
닫기
    인기검색어 순위 펼치기

    RISS 인기검색어

      KCI등재

      Expression of DEK in Oral Squamous Cell Carcinoma

      한글로보기

      https://www.riss.kr/link?id=A106895470

      • 0

        상세조회
      • 0

        다운로드
      서지정보 열기
      • 내보내기
      • 내책장담기
      • 공유하기
      • 오류접수

      부가정보

      다국어 초록 (Multilingual Abstract)

      Human DEK gene on chromosome 6p encodes a 43kD nuclear phospoprotein that was originally identified as part of a fusion protein found in a subset of acute myeloid leukemia carrying a t(6;9) translocation. Although DEK upregulation has been described in a number of human malignancies and was significantly associated with high histologic grade, lymph node metastasis and/or advanced clinical stage, no previous report has evaluated the expression of DEK protein and its clinical significance in oral squamous cell carcinoma (OSCC). Our aims were to determine DEK expression in tissue samples of normal oral mucosa and OSCC by immunohistochemistry, to analyze the correlation between DEK expression and clinicopathological parameters, and to evaluate the value of DEK as a prognostic marker for patient’s survival. Ten normal oral mucosa, 10 epithelial dysplasia, and 60 OSCC samples were studied by immunohistochemistry. DEK expression tended to increase through the full thickness of epithelium in the dysplastic mucosa when compared with those in normal oral mucosa. High expression of DEK protein (score ≥ 2) was found in 68.3% of OSCC cases. Statistical analysis revealed that DEK overexpression in OSCC was positively correlated with high histologic grade (p=0.001), lymph node metastasis (p=0.003), and advanced clinical stage (p=0.039). In the Kaplan-Meier survival analysis, DEK overexpression was significantly associated with decreased overall survival in patients with OSCC (p=0.019). Our results suggest that DEK overexpression may be a reliable marker to predict the clinical outcome in OSCC.
      번역하기

      Human DEK gene on chromosome 6p encodes a 43kD nuclear phospoprotein that was originally identified as part of a fusion protein found in a subset of acute myeloid leukemia carrying a t(6;9) translocation. Although DEK upregulation has been described i...

      Human DEK gene on chromosome 6p encodes a 43kD nuclear phospoprotein that was originally identified as part of a fusion protein found in a subset of acute myeloid leukemia carrying a t(6;9) translocation. Although DEK upregulation has been described in a number of human malignancies and was significantly associated with high histologic grade, lymph node metastasis and/or advanced clinical stage, no previous report has evaluated the expression of DEK protein and its clinical significance in oral squamous cell carcinoma (OSCC). Our aims were to determine DEK expression in tissue samples of normal oral mucosa and OSCC by immunohistochemistry, to analyze the correlation between DEK expression and clinicopathological parameters, and to evaluate the value of DEK as a prognostic marker for patient’s survival. Ten normal oral mucosa, 10 epithelial dysplasia, and 60 OSCC samples were studied by immunohistochemistry. DEK expression tended to increase through the full thickness of epithelium in the dysplastic mucosa when compared with those in normal oral mucosa. High expression of DEK protein (score ≥ 2) was found in 68.3% of OSCC cases. Statistical analysis revealed that DEK overexpression in OSCC was positively correlated with high histologic grade (p=0.001), lymph node metastasis (p=0.003), and advanced clinical stage (p=0.039). In the Kaplan-Meier survival analysis, DEK overexpression was significantly associated with decreased overall survival in patients with OSCC (p=0.019). Our results suggest that DEK overexpression may be a reliable marker to predict the clinical outcome in OSCC.

      더보기

      참고문헌 (Reference)

      1 von Lindern M, "The translocation(6;9), associated with a specific subtype of acute myeloid leukemia, results in the fusion of two genes, dek and can, and the expression of a chimeric, leukemia-specific dek-can mRNA" 12 : 1687-1697, 1992

      2 Kroes RA, "The identification of novel therapeutic targets for the treatment of malignant brain tumors" 156 : 191-198, 2000

      3 Wise-Draper TM, "Overexpre-ssion of the cellular DEK protein promotes epithelial transformation in vitro and in vivo" 69 : 1792-1799, 2009

      4 Khodadoust MS, "Melanoma proliferation and chemoresistance controlled by the DEK oncogene" 69 : 6405-6413, 2009

      5 Lin L, "Mechanisms underlying cancer growth and apoptosis by DEK overexpression in colorectal cancer" 9 : e111260-, 2014

      6 Nagpal JK, "Identification of differentially expressed genes in tobacco chewing-mediated oral cancer by differential display-polymerase chain reaction" 37 : 658-664, 2007

      7 Kondoh N, "Identification and characterization of genes associated with human hepatocellular carcinogenesis" 59 : 4990-4996, 1999

      8 Piao J, "High expression of DEK predicts poor prognosis of gastric adenocarcinoma" 9 : 67-, 2014

      9 Grasemann C, "Gains and overexpression identify DEK and E2F3 as targets of chromosome 6p gains in retinoblastoma" 24 : 6441-6449, 2005

      10 Ferlay J, "GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11" International Agency for Research on Cancer

      1 von Lindern M, "The translocation(6;9), associated with a specific subtype of acute myeloid leukemia, results in the fusion of two genes, dek and can, and the expression of a chimeric, leukemia-specific dek-can mRNA" 12 : 1687-1697, 1992

      2 Kroes RA, "The identification of novel therapeutic targets for the treatment of malignant brain tumors" 156 : 191-198, 2000

      3 Wise-Draper TM, "Overexpre-ssion of the cellular DEK protein promotes epithelial transformation in vitro and in vivo" 69 : 1792-1799, 2009

      4 Khodadoust MS, "Melanoma proliferation and chemoresistance controlled by the DEK oncogene" 69 : 6405-6413, 2009

      5 Lin L, "Mechanisms underlying cancer growth and apoptosis by DEK overexpression in colorectal cancer" 9 : e111260-, 2014

      6 Nagpal JK, "Identification of differentially expressed genes in tobacco chewing-mediated oral cancer by differential display-polymerase chain reaction" 37 : 658-664, 2007

      7 Kondoh N, "Identification and characterization of genes associated with human hepatocellular carcinogenesis" 59 : 4990-4996, 1999

      8 Piao J, "High expression of DEK predicts poor prognosis of gastric adenocarcinoma" 9 : 67-, 2014

      9 Grasemann C, "Gains and overexpression identify DEK and E2F3 as targets of chromosome 6p gains in retinoblastoma" 24 : 6441-6449, 2005

      10 Ferlay J, "GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11" International Agency for Research on Cancer

      11 Evans AJ, "Defining a 0.5-mb region of genomic gain on chromosome 6p22in bladder cancer by quantitative-multiplex polymerase chain reaction" 164 : 285-293, 2004

      12 Wise-Draper TM, "DEK proto-oncogene expression interferes with the normal epithelial differentiation program" 174 : 71-81, 2009

      13 Liu S, "DEK overexpression is correlated with the clinical features of breast cancer" 62 : 176-181, 2012

      14 Wu Q, "DEK overexpression in uterine cervical cancers" 58 : 378-382, 2008

      15 Lin L, "DEK over expression as an independent biomarker for poor prognosis in colorectal cancer" 13 : 366-, 2013

      16 Carro MS, "DEK expression is controlled by E2F and deregulated in diverse tumor types" 5 : 1202-1207, 2006

      17 Patel RM, "DEK expression in Merkel cell carcinoma and small cell carcinoma" 39 : 753-757, 2012

      18 Han S, "Clinicopathological significance of DEK overexpression in serous ovarian tumors" 59 : 443-447, 2009

      19 Wise-Draper TM, "Apoptosis inhibition by the human DEK oncoprotein involves interference with p53 functions" 26 : 7506-7519, 2006

      더보기

      동일학술지(권/호) 다른 논문

      동일학술지 더보기

      더보기

      분석정보

      View

      상세정보조회

      0

      Usage

      원문다운로드

      0

      대출신청

      0

      복사신청

      0

      EDDS신청

      0

      동일 주제 내 활용도 TOP

      더보기

      주제

      연도별 연구동향

      연도별 활용동향

      연관논문

      연구자 네트워크맵

      공동연구자 (7)

      유사연구자 (20) 활용도상위20명

      인용정보 인용지수 설명보기

      학술지 이력

      학술지 이력
      연월일 이력구분 이력상세 등재구분
      2026 평가예정 재인증평가 신청대상 (재인증)
      2020-01-01 평가 등재학술지 유지 (재인증) KCI등재
      2017-01-01 평가 등재학술지 유지 (계속평가) KCI등재
      2013-01-01 평가 등재 1차 FAIL (등재유지) KCI등재
      2010-07-27 학술지명변경 한글명 : 대한구강악안면병리학회 -> 대한구강악안면병리학회지 KCI등재
      2010-01-01 평가 등재학술지 유지 (등재유지) KCI등재
      2007-01-01 평가 등재학술지 선정 (등재후보2차) KCI등재
      2006-01-01 평가 등재후보 1차 PASS (등재후보1차) KCI등재후보
      2005-01-01 평가 등재후보학술지 유지 (등재후보1차) KCI등재후보
      2003-01-01 평가 등재후보학술지 선정 (신규평가) KCI등재후보
      더보기

      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
      더보기

      이 자료와 함께 이용한 RISS 자료

      나만을 위한 추천자료

      해외이동버튼