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NF-κB、EGFR在肝内胆管结石合并肝内胆管癌组织的表达和意义 被引量:4

Expressions and Significances of NF-κB and EGFR in Hepatolithiasis Associated with Intrahepatic Cholangiocarcinoma
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摘要 目的探讨NF-κB和EGFR在肝内胆管结石合并肝内胆管癌组织的表达和意义。方法取中山大学附属第二医院1989年8月至2009年6月期间手术切除肝组织石蜡标本共90例,其中肝内胆管结石合并肝内胆管癌33例为观察组,单纯肝内胆管结石32例为对照组,正常肝内胆管组织25例为正常对照组。采用免疫组化SP法检测胆管细胞中NF-κB及EGFR表达情况,并分析其与肝内胆管结石合并肝内胆管癌临床病理特征及生存率的关系。结果从正常对照组、对照组到观察组,NF-κB与EGFR的表达阳性率逐渐升高(P<0.05,P<0.01)。EGFR的表达与肿瘤分化程度及肿瘤浸润深度有关(P<0.05),与患者的性别、年龄及淋巴结转移无关(P>0.05);NF-κB的表达与上述因素均无关(P>0.05)。肿瘤患者中EGFR呈阳性表达者,其累积生存率较低(P<0.01)。结论 NF-κB的异常表达是肝内胆管癌的早期事件,NF-κB与EGFR过表达在肝内胆管结石致胆管癌的癌变过程中起着协同的重要的作用,EGFR的过表达与肿瘤恶性程度和预后有关。 Objective To investigate the roles of NF-κB and EGFR in hepatolithiasis associated with intrahepatic cholangiocarcinoma.Methods Ninety cases of liver tissue specimens from hepatectomies performed in the 2nd Affiliated Hospital of Sun Yat-sen University between August 1989and June 2009were enrolled in the study.Among them,33cases of hepatolithiasis associated with intrahepatic cholangiocarcinoma were considered as observing group,32cases of hepatolithiasis as control group,and 25cases of normal bile duct tissues as normal control group.The SP method of immunohistochemical staining was applied to detect the expressions of NF-κB and EGFR in intrahepatic biliary ducts epithelial cells,and their relations with clinicopathologic factors and the accumulated survival rate of hepatolithiasis associated with intrahepatic cholangiocarcinoma were analyzed.Results Expression rates of NF-κB and EGFR were gradually raised from normal control group,control group to observing group(P0.01).Expression of EGFR in tumor patients was related to histopathologic differentiation grading and the depth of tumor invasion(P0.05),but not to gender,age,or lymph node metastasis(P0.05);there were no significant relationships between the expression of NF-κB and factors described above(P0.05).The survival rate of patients with tumor expressed EGFR was significantly lower than that of patients with tumor non-expressed EGFR(P0.01).Conclusions NF-κB expression is in the early stage during intrahepatic cholangiocarcinoma genesis.NF-κB and EGFR play cooperating roles during hepatolithiasis carcinogenesis process.Over expression of EGFR is related with poor differentiation and prognosis of tumor.
出处 《中国普外基础与临床杂志》 CAS 2010年第11期1158-1163,共6页 Chinese Journal of Bases and Clinics In General Surgery
关键词 核因子ΚB 表皮生长因子受体 胆结石 胆管癌 肝内 Nuclear factor kappa B Epidermal growth factor receptor Cholelithiasis Cholangiocarcinoma Intrahepatic
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参考文献21

  • 1虞积耀,崔全才主译.消化系统肿瘤病理学和遗传学分册·世界卫生组织肿瘤分类及诊断标准系列图书[M].北京:人民卫生出版社;2006:210-217.
  • 2Gores GJ.Cholangiocarcinoma:current concepts and insights[J].Hepatology,2003,37(5):961-969.
  • 3Malhi H.Gores GJ.Cholangiocarcinoma:modern advances in understanding a deadly old disease[J].J Hepatol,2006; 45(6):856-867.
  • 4Sugawara H.Yasoshima M,Katayanagi K,et al.Relationship between interleukin-6 and proliferation and differentiation in cholangiocarcinoma.[J].Histopathology,1998; 33 (2):145-153.
  • 5Kobayashi S,Werneburg NW,Bronk SF,et al.Interleukin-6 contributes to Mcl-1 up-regulation and TRAIL resistance via an Akt-signaling pathway in cholangiocarcinoma cells[J].Gastroenterology,2005; 128(7).2054-2065.
  • 6Isomoto H,Mott JL,Kobayashi S,et al.Sustained IL-6/ STAT-3 signaling in cholangiocarcinoma cells due to SOCS-3 epigenetic silencing[J].Gastroenterology,2007;132(1):384-396.
  • 7Yoon JH,Werneburg NW,Higuchi H,et al.Bile acids inhibit Mcl-1 protein turnover via an epidermal growth factor receptor/Raf-1-dependent mechanism[J].Cancer Res,2002; 62(22):6500-6505.
  • 8Werneburg NW,Yoon JH,Higuchi H,et al.Bile acids activate EGF receptor via a TGF-alpha-dependent mechanism in human cholangiocyte cell lines[J].Am J Physiol Gastroint-est Liver Physiol,2003; 285(1):G31-G36.
  • 9Yamagiwa Y,Meng F,Patel T.Interleukin-6 decreases senescence and increases telomerase activity in malignant human cholangiocytes[J].Life Sci,2006; 78(21):2494-2502.
  • 10Andrzejewska A,Jurkowska G.Nitric oxide protects the ul-trastructure of pancreatic acinar cells in the course of caer-ulein-induced acute pancreatitis[J].Int J Exp Pathol,1999; 80(6):317-324.

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  • 1IoannisHatzaras,CarlSchmidt,PeterMuscarella,W. ScottMelvin,E. ChristopherEllison,MarkBloomston.Elevated CA 19‐9 portends poor prognosis in patients undergoing resection of biliary malignancies[J].HPB.2010(2)
  • 2SibuleskyL,NguyenJ,PatelT.Preneoplasticconditionsun-derlyingbileductcancer[J].LangenbecksArchSurg,2012,397(6):861-867.
  • 3ChenS,XiongJ,ZhanY,etal.InhibitsLPS-inducedinflam-matoryresponsesinratdorsalrootganglionneuronsviain-hibitingTLR4-MyD88-TAK1-MediatedNF-κB andMAPKsignalingpathway[J].CellMolNeurobiol,2015,35(4):523-531.
  • 4ZhangS,YangN,NiS,etal.Pretreatmentoflipopolysaccha-ride(LPS) amelioratesD-GalN/LPSinducedacuteliverfailurethroughTLR4signalingpathway[J].IntJClinExpPathol,2014,7(10):6626-6634.
  • 5ParkMY,MunST.CarnosicacidinhibitsTLR4-MyD88sig-nalingpathwayinLPS-stimulated3T3-L1adipocytes[J].Nu-trResPract,2014,8(5):516-520.
  • 6NesaretnamK, Meganathan P.Tocotrienols:inflammationandcancer[J].AnnNYAcadSci,2011,1229(1):18-22.
  • 7AggarwalBB,SungB.Therelationshipbetweeninflammationandcancerisanalogoustothatbetweenfuelandfire[J].On-cology(WillistonPark),2011,25(5):414-418.
  • 8ZamarronBF,ChenW.Dualrolesofimmunecellsandtheirfactorsincancerdevelopmentandprogression[J].IntJBiolSci.2011,7(5):651-658.
  • 9SiobhanS,ElizabethA.Inflammationandprostatecancer:afocusoninfections[J].CurrUrolRep,2008,9(3):243-249.
  • 10GoswamiB,RajappaM,SharmaM,etal.Inflammation:itsroleandinterplayinthedevelopmentofcancer,withspecialfocusongynecologicalmalignancies[J].IntJGynecolCanc-er,2008,18(4):591-599.

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