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    Expression and mutational analysis of TGF-β/Smads signaling in human cervical cancers

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    https://www.riss.kr/link?id=A104778002

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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    Objective: To define the molecular basis of TGF-β1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-β1, TGF-β1 receptors, and Smads, the regulators of the TGF-β1 signaling pathway, in human cervical cancers.
    Methods: Expression of TGF-β1, TGF-β1 receptors, and Smads transcripts were determined by quantitative reverse transcription-polymerase chain reaction (RT-PCR), and sequence alteration was analyzed using RT-PCR-single-strand conformation polymorphism (SSCP) analysis. Genomic levels of TGF-β1, TGF-β1 receptors and Smads was also measured by quantitative genomic PCR.
    Results: Abnormal overexpression of TGF-β1 and abnormal reduction of type II TGF-β1 receptor were identified in 36% (18 of 50) and 20% (10 of 50) of cervical cancer tissues, respectively. 22% (11 of 50) in Smad2 and 14% (7 of
    50) in Smad4 revealed tumor specific mRNA reduction less than a half of normal means. In addition, no evidence for sequence alterations of the gene was found by RT-PCR-SSCP analysis.
    Conclusion: Our study demonstrates that disruption of TGF-β/Smad signaling pathway exist in human cervical cancer, suggesting that abnormal expressions of the member of TGF-β/Smad signaling pathway might contribute to the malignant progression of human cervical tumors via suppressing the tumor suppression function of TGF-β1 1's tumor suppression function.
    번역하기

    Objective: To define the molecular basis of TGF-β1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-β1, TGF-β1 receptors, and Smads, the regulators of the TGF-β1 signaling pathway, in human cervical canc...

    Objective: To define the molecular basis of TGF-β1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-β1, TGF-β1 receptors, and Smads, the regulators of the TGF-β1 signaling pathway, in human cervical cancers.
    Methods: Expression of TGF-β1, TGF-β1 receptors, and Smads transcripts were determined by quantitative reverse transcription-polymerase chain reaction (RT-PCR), and sequence alteration was analyzed using RT-PCR-single-strand conformation polymorphism (SSCP) analysis. Genomic levels of TGF-β1, TGF-β1 receptors and Smads was also measured by quantitative genomic PCR.
    Results: Abnormal overexpression of TGF-β1 and abnormal reduction of type II TGF-β1 receptor were identified in 36% (18 of 50) and 20% (10 of 50) of cervical cancer tissues, respectively. 22% (11 of 50) in Smad2 and 14% (7 of
    50) in Smad4 revealed tumor specific mRNA reduction less than a half of normal means. In addition, no evidence for sequence alterations of the gene was found by RT-PCR-SSCP analysis.
    Conclusion: Our study demonstrates that disruption of TGF-β/Smad signaling pathway exist in human cervical cancer, suggesting that abnormal expressions of the member of TGF-β/Smad signaling pathway might contribute to the malignant progression of human cervical tumors via suppressing the tumor suppression function of TGF-β1 1's tumor suppression function.

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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    Objective: To define the molecular basis of TGF-β1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-β1, TGF-β1 receptors, and Smads, the regulators of the TGF-β1 signaling pathway, in human cervical cancers.
    Methods: Expression of TGF-β1, TGF-β1 receptors, and Smads transcripts were determined by quantitative reverse transcription-polymerase chain reaction (RT-PCR), and sequence alteration was analyzed using RT-PCR-single-strand conformation polymorphism (SSCP) analysis. Genomic levels of TGF-β1, TGF-β1 receptors and Smads was also measured by quantitative genomic PCR.
    Results: Abnormal overexpression of TGF-β1 and abnormal reduction of type II TGF-β1 receptor were identified in 36% (18 of 50) and 20% (10 of 50) of cervical cancer tissues, respectively. 22% (11 of 50) in Smad2 and 14% (7 of
    50) in Smad4 revealed tumor specific mRNA reduction less than a half of normal means. In addition, no evidence for sequence alterations of the gene was found by RT-PCR-SSCP analysis.
    Conclusion: Our study demonstrates that disruption of TGF-β/Smad signaling pathway exist in human cervical cancer, suggesting that abnormal expressions of the member of TGF-β/Smad signaling pathway might contribute to the malignant progression of human cervical tumors via suppressing the tumor suppression function of TGF-β1 1's tumor suppression function.
    번역하기

    Objective: To define the molecular basis of TGF-β1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-β1, TGF-β1 receptors, and Smads, the regulators of the TGF-β1 signaling pathway, in human cervical canc...

    Objective: To define the molecular basis of TGF-β1 function in cervical carcinogenesis, we explored the expression and mutational status of TGF-β1, TGF-β1 receptors, and Smads, the regulators of the TGF-β1 signaling pathway, in human cervical cancers.
    Methods: Expression of TGF-β1, TGF-β1 receptors, and Smads transcripts were determined by quantitative reverse transcription-polymerase chain reaction (RT-PCR), and sequence alteration was analyzed using RT-PCR-single-strand conformation polymorphism (SSCP) analysis. Genomic levels of TGF-β1, TGF-β1 receptors and Smads was also measured by quantitative genomic PCR.
    Results: Abnormal overexpression of TGF-β1 and abnormal reduction of type II TGF-β1 receptor were identified in 36% (18 of 50) and 20% (10 of 50) of cervical cancer tissues, respectively. 22% (11 of 50) in Smad2 and 14% (7 of
    50) in Smad4 revealed tumor specific mRNA reduction less than a half of normal means. In addition, no evidence for sequence alterations of the gene was found by RT-PCR-SSCP analysis.
    Conclusion: Our study demonstrates that disruption of TGF-β/Smad signaling pathway exist in human cervical cancer, suggesting that abnormal expressions of the member of TGF-β/Smad signaling pathway might contribute to the malignant progression of human cervical tumors via suppressing the tumor suppression function of TGF-β1 1's tumor suppression function.

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    참고문헌 (Reference)

    1 Markowitz SD, "Tumor suppressor activity of the TGF-beta pathway in human cancers" 7 : 93-102, 1996

    2 Kim JW, "Transforming growth factor-β1 induces apoptosis through down-regulation of c-mycGene and overexpression of p27Kip1 protein in cervical carcinoma" 69 : 230-236, 1998

    3 Chen T, "Transforming growth factor-beta receptor type I gene is frequently mutated in ovarian carcinomas" 61 : 4679-4682, 2001

    4 Welch DR, "Transforming growth factor beta stimulates mammary adenocarcinoma cell invasion and metastatic potential" 87 : 7678-7682, 1990

    5 Kang SH, "Transcriptional repression of the transforming growth factor-beta type I receptor gene by DNA methylation results in the development of TGF-beta resistance in human gastric cancer" 18 : 7280-7286, 1999

    6 Derynck R, "TGF-beta signaling in tumor suppression and cancer progression" 29 : 117-129, 2001

    7 Massague J, "TGF-beta signal transduction" 67 : 753-791, 1998

    8 Liu X, "Ski/Sno and TGF-beta signaling" 12 : 1-8, 2001

    9 Pasche B, "Role of transforming growth factor beta in cancer" 186 : 153-168, 2001

    10 Hazelbag S, "Overexpression of the alpha v beta 6 integrin in cervical squamous cell carcinoma is a prognostic factor for decreased survival" 212 : 316-324, 2007

    1 Markowitz SD, "Tumor suppressor activity of the TGF-beta pathway in human cancers" 7 : 93-102, 1996

    2 Kim JW, "Transforming growth factor-β1 induces apoptosis through down-regulation of c-mycGene and overexpression of p27Kip1 protein in cervical carcinoma" 69 : 230-236, 1998

    3 Chen T, "Transforming growth factor-beta receptor type I gene is frequently mutated in ovarian carcinomas" 61 : 4679-4682, 2001

    4 Welch DR, "Transforming growth factor beta stimulates mammary adenocarcinoma cell invasion and metastatic potential" 87 : 7678-7682, 1990

    5 Kang SH, "Transcriptional repression of the transforming growth factor-beta type I receptor gene by DNA methylation results in the development of TGF-beta resistance in human gastric cancer" 18 : 7280-7286, 1999

    6 Derynck R, "TGF-beta signaling in tumor suppression and cancer progression" 29 : 117-129, 2001

    7 Massague J, "TGF-beta signal transduction" 67 : 753-791, 1998

    8 Liu X, "Ski/Sno and TGF-beta signaling" 12 : 1-8, 2001

    9 Pasche B, "Role of transforming growth factor beta in cancer" 186 : 153-168, 2001

    10 Hazelbag S, "Overexpression of the alpha v beta 6 integrin in cervical squamous cell carcinoma is a prognostic factor for decreased survival" 212 : 316-324, 2007

    11 Lynch MA, "Mutational analysis of the transforming growth factor beta receptor type II gene in human ovarian carcinoma" 58 : 4227-4232, 1998

    12 Kim SJ, "Molecular mechanisms of inactivation of TGF-beta receptors during carcinogenesis" 11 : 159-168, 2000

    13 Shi Y, "Mechanisms of TGF-β signaling from cell membrane to the nucleus" 113 : 685-700, 2003

    14 Massague J, "How cells read TGF-beta signals" 1 : 169-178, 2000

    15 Kang SH, "Genetic integrity of transforming growth factor beta (TGF-beta) receptors in cervical carcinoma cell lines: loss of growth sensitivity but conserved transcriptional response to TGF-beta" 77 : 620-625, 1998

    16 Riggins GJ, "Frequency of Smad gene mutations in human cancers" 57 : 2578-2580, 1997

    17 Siegel PM, "Cytostatic and apoptotic actions of TGF-beta in homeostasis and cancer" 3 : 807-821, 2003

    18 Massague J, "Controlling TGF-beta signaling" 14 : 627-644, 2000

    19 Waggoner SE, "Cervical cancer" 361 : 2217-2225, 2003

    20 Hai-Rim Shin, "2002 Annual Report of the Korea Central Cancer Registry: Based on Registered Data from 139 Hospitals" 대한암학회 36 (36): 103-114, 2004

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    학술지 이력

    학술지 이력
    연월일 이력구분 이력상세 등재구분
    2023 평가 해외DB학술지평가 신청대상 (해외등재 학술지 평가)
    2020-01-01 등재 등재학술지 유지 (해외등재 학술지 평가) KCI등재
    2012-07-13 학회명변경 한글명 : 대한부인종양콜포스코피학회 -> 대한부인종양학회
    영문명 : Korean Society of Gynecologic Oncology and Colposcopy -> Korean Society of Gynecologic Oncology
    KCI등재
    2012-01-01 등재 등재학술지 선정 (등재후보2차) KCI등재
    2011-01-01 등재 등재후보 1차 PASS (등재후보1차) KCI등재후보
    2010-01-01 등재 등재후보학술지 유지 (등재후보2차) KCI등재후보
    2009-01-01 등재 등재후보 1차 PASS (등재후보1차) KCI등재후보
    2008-06-26 학술지명변경 한글명 : 부인종양 -> Journal of Gynecologic Oncology
    외국어명 : Korean Journal of Gynecologic Oncology -> Journal of Gynecologic Oncology
    KCI등재후보
    2008-01-01 등재 등재후보 1차 FAIL (등재후보1차) KCI등재후보
    2007-01-01 등재 등재후보학술지 유지 (등재후보1차) KCI등재후보
    2006-09-13 학술지명변경 한글명 : 대한부인종양.콜포스코피학회지 -> 부인종양
    외국어명 : 미등록 -> Korean Journal of Gynecologic Oncology
    KCI등재후보
    2005-01-01 등재 등재후보학술지 선정 (신규평가) KCI등재후보
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    기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
    2016 2.18 0.12 1.48
    KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
    1.13 0.9 0.732 0
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