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胆囊腺癌pAKT、VEGF、微血管和微淋巴生成的检测及其临床意义 被引量:2

Significance of pAKT、VEGF、 Intratumour MVD and MLD in gallbladder carcinomas
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摘要 目的研究胆囊腺癌组织中磷酸化丝氨酸/苏氨酸激酶(pAKT)、血管内皮生长因子(VEGF)蛋白的表达、微血管密度(MVD)和微淋巴管密度(MLD)及其临床意义。方法应用免疫组织化学SP法检测46例胆囊腺癌pAKT、VEGF、微血管和微淋巴管密度。结果胆囊腺癌pAKT和VEGF的阳性表达率分别为87.0%(40/46)和91.3%(42/46)。pAKT的阳性表达与临床分期和淋巴结转移显著相关,统计学有显著性差异(P<0.05)。MVD与肿瘤生长方式和临床分期显著相关;MLD与肿瘤生长方式和淋巴结转移有非常显著差异(P<0.01)。pAKT和VEGF阳性组的MVD明显高于其阴性组,Spearman相关分析表明pAKT和VEGF表达与MVD呈正相关。pAKT阳性组的MLD明显高于阴性组,Spearman相关分析揭示pAKT表达与MLD呈正相关,而VEGF阳性组的MLD与阴性组之间无显著性差异。结论 pAKT和VEGF与胆囊腺癌发生发展和转移密切相关,这提示阻断PI3K/AKT信号传导通路将对胆囊腺癌的治疗提供新的靶点。 Objective Methods Conclusion To study effect of expression of phosphorylated AKT(pAKT),vascular endothyelial growth factor(VEGF) and on intratumour microvessel density(MVD),microlymphatic density(MLD) in gallbladder carcinoma tissues.Methods Immunohistochemical method was used to detect the expressions of pAKT,VEGF,MVD,and MLD in 46 gallbladder carcinomas.Results The positive expression rates of pAKT and VEGF of gallbladder carcinoma were 87.0%(40/46)and 91.3%(42/46)respectively.The positive expression of pAKT was correlated to clinical staging and lymph node metastasis.The MVD was closely related to clinical staging and growth style.The MLD was associated with growth style and lymph node metastasis.The expression of pAKT and VEGF was positively correlation.Conclusion The results shown that pAKT and VEGF are might had important significance in the carcinogenesis,progression,and metastasis of gallbladder carcinoma,it might be as a potentially useful target for therapeutic intervention in gallbladder carcinoma patients.
出处 《中国实验诊断学》 北大核心 2011年第7期1089-1092,共4页 Chinese Journal of Laboratory Diagnosis
基金 广东省深圳市科技局项目(201003322)
关键词 胆囊肿瘤 磷酸化丝氨酸/苏氨酸激酶 血管内皮生长因子 微血管 微淋巴管密 转移 Gallbladder neoplasms pAKT VEGF microvessel Microlymphatic Metastasis
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参考文献11

  • 1周晓东,于皆平,于红刚,罗和生,吕农华,朱萱.蛋白激酶B在胃癌中的表达及其生物学意义[J].中华消化杂志,2005,25(7):401-405. 被引量:21
  • 2Yamamoto K, Tomita Y, Hoshida J, et al. Prognostic significance of acti- vated AKT expression in pancreatic ductal adenocarcinoma [J]. Clin Can- cer Res,2004,10(8) :2846.
  • 3Grabacka M, Plonka PM, Urbanska K, et al. Peroxisome proliferator-acti- vated receptor alpha activation decreases metastatic potential of melanoma cells in vitro via down-regulation of Akt [J]. Clin Cancer Res. 2006, 12(10):3028.
  • 40ka N,Tanirmto S,Taue R, et al. Role ff phosphatidylinositol 3-kinase/Akt pathway in bladder caneer cell apoptosis induced by tumor necrosis factor-re- lated apoptosis-indueing ligand[J]. Cancer Sei,20C6,97(10) : 1(/93.
  • 5Shinohara M, Chung YJ, Saji M, et al. AKT in thyroid tumorigenesis and progression [ J ]. Endocrinology 2007,148 (3) : 942.
  • 6Kajiya K,Hirakawa S, Ma B, et al. Hepatocyte growth factor prtrnotes lym- phatic vessel forrmti~n and function [J] .EMBO J,2005,24(16):2885.
  • 7Jiang WG, Davies G, Martin TA, et al. The Potential lymphangiogenic ef- fects of hepatocyte growth factor/scatter factor in vitro and in vivo [J]. Int J Mol Med,2005,16(4) :723.
  • 8Kobayashi I, Semba S, Matsuda Y, et al. Significance of Akt phosphoryla-tion on tumor growth and vascular endothelial growth factor expression in human gastric carcinoma[ J]. Pathobiology 2006,73( 1 ) :8.
  • 9Hu L, Hofmann J,Jaffe RB. Phosphafidylinositol 3-kinase mediates angio- genesis and vascular permeability associated with ovarian carcinoma [J]. Clin Cancer Res 2005,11 (22) : 8208.
  • 10Agarwal A,Das K, Lemer N,Sathe S,et al.The AKT/I? B kinase path- way promotes angiogenic/metastatic gene expression in colorectal cancer by activating nuclear factor-roB and 13-catenin [ J 1. oncogene, 2005,24 (6) :1021.

二级参考文献16

  • 1Dudek H, Datta SR, Franke TF, et al. Regulation of neuronal survival by the serine-threonine protein kinase Akt. Science,1997,275:661-665.
  • 2Burgering BM, Coffer PJ. Protein kinase B(c-Akt) in phosphatidylinositol-3-OH kinase signal transduction. Nature,1995,376: 599-602.
  • 3Schlieman MG, Fahy BN, Ramsamooj R, et al. Incidence,mechanism and prognostic value of activated AKT in pancreas cancer. Br J Cancer, 2003,89:2110-2115.
  • 4Ringel MD, Hayre N, Saito J, et al. Overexpression and overactivation of Akt in thyroid carcinoma. Cancer Res, 2001, 61:6105-6111.
  • 5Itoh N, Semba S, Ito M, et al. Phosphorylation of Akt/PKB is required for suppression of cancer cell apoptosis and tumor progression in human colorectal carcinoma. Cancer, 2002,94:3127-3134.
  • 6Liu AX, Testa JR, Hamilton TC, et al. AKT2, a member of the protein kinase B family, is activated by growth factors,v-Ha-fas, and v-src through phosphatidylinositol 3-kinase in human ovarian epithelial cancer cells. Cancer Res, 1998, 58:2973-2977.
  • 7Sambrook J, Fritsch EF, Maniatis T, eds Molecular cloning: A laboratory manual, 2nd ed. New York: Cold Spring Harbor Laboratory Press, 1989.
  • 8Perez-Tenorio G, Stal O. Activation of AKT/PKB in breast cancer predicts a worse outcome among endocrine treated patients. Br J Cancer, 2002,86:540-545.
  • 9Terakawa N, Kanamori Y, Yoshida S. Loss of PTEN expression followed by Akt phosphorylation is a poor prognostic factor for patients with endometrial cancer. Endocr Relat Cancer,2003, 10:203-208.
  • 10Fresno Vara JA, Casado E, de Castro J, et al. PI3K/Akt signalling pathway and cancer. Cancer Treat Rev, 2004, 30: 193-204.

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