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    L1 Cell Adhesion Molecule Expression Is Associated With Pelvic Lymph Node Metastasis and Advanced Stage in Diabetic Patients With Endometrial Cancer: A Matched Case Control Study

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    https://www.riss.kr/link?id=A104785932

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    다국어 초록 (Multilingual Abstract) kakao i 다국어 번역

    Background: Diabetic patients with endometrial cancer had more lymph node metastasis than non-diabetic patients with endometrial cancer. L1 cell adhesion molecule (L1CAM) could be possibly associated with lymph node metastasis in diabetic patients with endometrial cancer via epithelial-mesenchymal transition. We aimed to investigate the association between L1CAM expression and lymph node metastasis in diabetic patients with endometrial cancer.
    Methods: We conducted a matched case control study of 68 endometrial cancer patients who comprise each 34 diabetic and non-diabetic patients. L1CAM expression was evaluated by immunohistochemistry using fresh formalin-fixed paraffin-embedded tissue block of the patients. The association between L1CAM expression and pelvic lymph node metastasis was assessed according to the presence of diabetes.
    Results: Of the 68 patients, 13 (19.1%) were positive for L1CAM immunostaining. Positive rate of L1CAM expression in diabetic endometrial cancer patients was similar to that in non-diabetic endometrial cancer patients (14.7% vs. 23.5%, P = 0.355). Tumor recurred more frequently in patients with positive L1CAM expression than those with negative L1CAM expression (33.3% vs. 1.6%, P = 0.019). However, we failed to find any significant association between L1CAM expression and lymph node metastasis. Only for the diabetic patients (n = 34), patients with pelvic lymph node metastasis had more L1CAM expression than those without lymph node metastasis (50.0% vs. 3.6%, P = 0.035). Advanced stage was the only risk factor for recurrence that showed a significant association with L1CAM expression for the diabetic endometrial cancer patients (P = 0.006), as well as all the enrolled patients (P = 0.014).
    Conclusion: L1CAM expression is associated with pelvic lymph node metastasis and advanced stage in diabetic patients with endometrial cancer.
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    Background: Diabetic patients with endometrial cancer had more lymph node metastasis than non-diabetic patients with endometrial cancer. L1 cell adhesion molecule (L1CAM) could be possibly associated with lymph node metastasis in diabetic patients wit...

    Background: Diabetic patients with endometrial cancer had more lymph node metastasis than non-diabetic patients with endometrial cancer. L1 cell adhesion molecule (L1CAM) could be possibly associated with lymph node metastasis in diabetic patients with endometrial cancer via epithelial-mesenchymal transition. We aimed to investigate the association between L1CAM expression and lymph node metastasis in diabetic patients with endometrial cancer.
    Methods: We conducted a matched case control study of 68 endometrial cancer patients who comprise each 34 diabetic and non-diabetic patients. L1CAM expression was evaluated by immunohistochemistry using fresh formalin-fixed paraffin-embedded tissue block of the patients. The association between L1CAM expression and pelvic lymph node metastasis was assessed according to the presence of diabetes.
    Results: Of the 68 patients, 13 (19.1%) were positive for L1CAM immunostaining. Positive rate of L1CAM expression in diabetic endometrial cancer patients was similar to that in non-diabetic endometrial cancer patients (14.7% vs. 23.5%, P = 0.355). Tumor recurred more frequently in patients with positive L1CAM expression than those with negative L1CAM expression (33.3% vs. 1.6%, P = 0.019). However, we failed to find any significant association between L1CAM expression and lymph node metastasis. Only for the diabetic patients (n = 34), patients with pelvic lymph node metastasis had more L1CAM expression than those without lymph node metastasis (50.0% vs. 3.6%, P = 0.035). Advanced stage was the only risk factor for recurrence that showed a significant association with L1CAM expression for the diabetic endometrial cancer patients (P = 0.006), as well as all the enrolled patients (P = 0.014).
    Conclusion: L1CAM expression is associated with pelvic lymph node metastasis and advanced stage in diabetic patients with endometrial cancer.

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    참고문헌 (Reference)

    1 Huszar M, "Up-regulation of L1CAM is linked to loss of hormone receptors and E-cadherin in aggressive subtypes of endometrial carcinomas" 220 : 551-561, 2010

    2 Geismann C, "Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer" 69 : 4517-4526, 2009

    3 Shergill IS, "Tissue microarrays: a current medical research tool" 20 : 707-712, 2004

    4 Jawhar NM, "Tissue microarray: a rapidly evolving diagnostic and research tool" 29 : 123-127, 2009

    5 Zecchini S, "The differential role of L1 in ovarian carcinoma and normal ovarian surface epithelium" 68 : 1110-1118, 2008

    6 Hills CE, "TGF-beta1-induced epithelial-to-mesenchymal transition and therapeutic intervention in diabetic nephropathy" 31 : 68-74, 2010

    7 Chung HH, "Role of integrated PET-CT in pelvic lymph node staging of cervical cancer before radical hysterectomy" 67 : 61-66, 2009

    8 Holian J, "Role of Kruppel-like factor 6 in transforming growth factor-beta1-induced epithelial-mesenchymal transition of proximal tubule cells" 295 : F1388-F1396, 2008

    9 Pecorelli S, "Revised FIGO staging for carcinoma of the vulva, cervix, and endometrium" 105 : 103-104, 2009

    10 Kang S, "Preoperative identification of a low-risk group for lymph node metastasis in endometrial cancer: a Korean gynecologic oncology group study" 30 : 1329-1334, 2012

    1 Huszar M, "Up-regulation of L1CAM is linked to loss of hormone receptors and E-cadherin in aggressive subtypes of endometrial carcinomas" 220 : 551-561, 2010

    2 Geismann C, "Up-regulation of L1CAM in pancreatic duct cells is transforming growth factor beta1- and slug-dependent: role in malignant transformation of pancreatic cancer" 69 : 4517-4526, 2009

    3 Shergill IS, "Tissue microarrays: a current medical research tool" 20 : 707-712, 2004

    4 Jawhar NM, "Tissue microarray: a rapidly evolving diagnostic and research tool" 29 : 123-127, 2009

    5 Zecchini S, "The differential role of L1 in ovarian carcinoma and normal ovarian surface epithelium" 68 : 1110-1118, 2008

    6 Hills CE, "TGF-beta1-induced epithelial-to-mesenchymal transition and therapeutic intervention in diabetic nephropathy" 31 : 68-74, 2010

    7 Chung HH, "Role of integrated PET-CT in pelvic lymph node staging of cervical cancer before radical hysterectomy" 67 : 61-66, 2009

    8 Holian J, "Role of Kruppel-like factor 6 in transforming growth factor-beta1-induced epithelial-mesenchymal transition of proximal tubule cells" 295 : F1388-F1396, 2008

    9 Pecorelli S, "Revised FIGO staging for carcinoma of the vulva, cervix, and endometrium" 105 : 103-104, 2009

    10 Kang S, "Preoperative identification of a low-risk group for lymph node metastasis in endometrial cancer: a Korean gynecologic oncology group study" 30 : 1329-1334, 2012

    11 Fujimoto T, "Para-aortic lymphadenectomy may improve disease-related survival in patients with multipositive pelvic lymph node stage IIIc endometrial cancer" 107 : 253-259, 2007

    12 Brummendorf T, "Neural cell recognition molecule L1: from cell biology to human hereditary brain malformations" 8 : 87-97, 1998

    13 Del Barco S, "Metformin: multi-faceted protection against cancer" 2 : 896-917, 2011

    14 Barrière G, "Metformin: a rising star to fight the epithelial mesenchymal transition in oncology" 13 : 333-340, 2012

    15 Hill EK, "Medical therapy of endometrial cancer: current status and promising novel treatments" 72 : 705-713, 2012

    16 Dong Hoon Suh, "Major clinical research advances in gynecologic cancer in 2011" 대한부인종양학회 23 (23): 53-64, 2012

    17 Pfeifer M, "L1CAM expression in endometrial carcinomas is regulated by usage of two different promoter regions" 11 : 64-, 2010

    18 Gavert N, "L1, a novel target of beta-catenin signaling, transforms cells and is expressed at the invasive front of colon cancers" 168 : 633-642, 2005

    19 Fogel M, "L1 expression as a predictor of progression and survival in patients with uterine and ovarian carcinomas" 362 : 869-875, 2003

    20 Boo YJ, "L1 expression as a marker for poor prognosis, tumor progression, and short survival in patients with colorectal cancer" 14 : 1703-1711, 2007

    21 Raveh S, "L1 cell adhesion molecule (L1CAM) in invasive tumors" 282 : 137-145, 2009

    22 Gast D, "L1 augments cell migration and tumor growth but not beta3integrin expression in ovarian carcinomas" 115 : 658-665, 2005

    23 Fogel M, "L1 (CD171) as a novel biomarker for ovarian and endometrial carcinomas" 4 : 455-462, 2004

    24 Steiner E, "Influence of diabetes mellitus and nodal distribution in endometrial cancer and correlation to clinico-pathological prognostic factors" 27 : 477-480, 2006

    25 Jiang H, "Identification of urinary soluble E-cadherin as a novel biomarker for diabetic nephropathy" 25 : 232-241, 2009

    26 Sengupta U, "Expression-based network biology identifies alteration in key regulatory pathways of type 2 diabetes and associated risk/complications" 4 : e8100-, 2009

    27 Park JY, "Comparison of the validity of magnetic resonance imaging and positron emission tomography/computed tomography in the preoperative evaluation of patients with uterine corpus cancer" 108 : 486-492, 2008

    28 Kitajima K, "Comparison of DWI and PET/CT in evaluation of lymph node metastasis in uterine cancer" 4 : 207-214, 2012

    29 Hills CE, "C-peptide reverses TGF-beta1-induced changes in renal proximal tubular cells: implications for treatment of diabetic nephropathy" 296 : F614-F621, 2009

    30 Weiderpass E, "Body size in different periods of life, diabetes mellitus, hypertension, and risk of postmenopausal endometrial cancer (Sweden)" 11 : 185-192, 2000

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    연월일 이력구분 이력상세 등재구분
    2022 평가 재인증평가 신청대상 (재인증)
    2019-01-01 등재 등재학술지 선정 (계속평가) KCI등재
    2018-12-01 등재 등재후보로 하락 (계속평가) KCI등재후보
    2015-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2013-10-14 학술지명변경 외국어명 : Cancer Prevention Research -> Journal of Cancer Prevention KCI등재
    2012-10-15 학회명변경 영문명 : Korean Association of Cancer Prevention -> Korean Society of Cancer Preveniton KCI등재
    2011-04-04 학술지명변경 외국어명 : Journal of Korean Association of Cancer Prevention -> Cancer Prevention Research KCI등재
    2011-01-01 등재 등재학술지 유지 (등재유지) KCI등재
    2008-01-01 등재 등재학술지 선정 (등재후보2차) KCI등재
    2007-01-01 등재 등재후보 1차 PASS (등재후보1차) KCI등재후보
    2005-01-01 등재 등재후보학술지 선정 (신규평가) KCI등재후보
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    기준연도 WOS-KCI 통합IF(2년) KCIF(2년) KCIF(3년)
    2016 0.22 0.22 0.18
    KCIF(4년) KCIF(5년) 중심성지수(3년) 즉시성지수
    0.15 0.12 0.405 0.13
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