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胃癌组织血小板衍化内皮细胞生长因子的表达与血管生成和凋亡的关系 被引量:1

Correlation of platelet-derived endothelial cell growth factor/Thymidine phosphorylase expression to angiogenesis and apoptosis in gastric carcinoma
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摘要 目的探讨血小板衍化内皮细胞生长因子(PD.ECGF)在胃癌组织中的表达及与血管生成和凋亡的关系。方法应用免疫组化技术对67例胃癌组织进行PD-ECGF表达、肿瘤组织微血管密度(MVD)检测,流式细胞技术检测胃癌组织细胞凋亡指数(川,凋亡百分率八结果*r***F的表达与胃癌淋巴结转移(P<0.oj)。分化程度(P<0.05)及组织分型(P<0.05)显著相关,与*V则尸<001)和胃癌细胞凋亡指数(P<001)显著相关。**D和*1与淋巳结转移(P<001)显著相关。结论胃癌组织中P*。ECGF可促进血管生成,抑制胃癌细胞凋亡,促进胃癌的增殖与转移。 Objective To investigate the relationship of the expression of platelet-derived endothelial cell growth fac-tor/Thymidine phosphorylase (PD-ECGF/TP) to angiogenesis and apoptosis in gastric carcinoma. Methods The expression of PD-ECGF and microvascular density (MVD) in gastric carcinoma was examined by immunohistochemical staining in 67 cases, apoptosis index (AI, percentage of apoptosis cells) in gastric carcinoma was examined by flow cytometry. Results There was a close correlation between PD-ECGF expression and several clinicopathological factors including lymph node metastasis ( P < 0.05), histology (P<0.05) and histological type ( P < 0.05) , and also a significant correlation with MVD (P<0.0l) and AI( P < 0.01) .MVD and AI were significantly correlated with lymph node metastasis ( P < 0.01) .Conclusions These findings indicated that the upregulation of PD-ECGF may stimulate angiogenesis and inhibit apoptosis in gastric carcinoma, accordingly influence tumor growth and metastasis.
出处 《胃肠病学和肝病学杂志》 CAS 2003年第2期165-168,共4页 Chinese Journal of Gastroenterology and Hepatology
关键词 胃癌组织 血小板 内皮细胞生长因子 细胞凋亡指数 胃癌 淋巴结转移 血管生成 Stomach neoplasms Platelet-derived endothelial cell growth factor Angiogenesis Apoptosis
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参考文献6

  • 1Fujioka S;Yoshida K;Yanagisawa S.Angiogenesis in pancreatic carcinoma[J],2001(92).
  • 2Takebayashi Y;Miyadera K;Akiyama S.Expression of thymidine phosphorylase in human gastric carcinoma,1996(03).
  • 3Matsushita S;Nitanda T;Furukawa T.The effect of a thymidine phosphorylase inhibitor on angiogenesis and apoptosis in tumors[J],1999(08).
  • 4Yoshikawa T;Suzuki K;Kobayashi O.Thymidinephosphorylase/platelet-derivedendothelialcellgrowthfactorisupregulatedinadvancedsolidtypesofgastriccancer[J],1999(79).
  • 5Osaki M;Sakatani T;Okamoto E.Thymidine phosphorylase expression results in a decrease in apoptosis and increase in intratumoral microvessel density in human gastric carcinomas[J],2000(01).
  • 6Ikeda R;Furukawa T;Kitazono M.Molecular basis for the inhibition of hypoxia-induced apoptosis by 2-deoxy-D-ribose[J],2002(04).

同被引文献13

  • 1Hengartner MO.The biochemistry of apoptosis,Nature,2000,407( ):770-775.
  • 2Bari R,Bedi A.Requirement of BAX for TRAIL/apo2L-induced apoptosis of colorectal cancers:synergism with sulindac-mediated inhibition of BclXL.Cancer Res,2002,62(6):1583-1587.
  • 3Greenstein S,Chias K,Krett NL.et al.Mechanisms of glucocorticoidmediated apoptosis in hematological malignancies.Clin Cancer Res,2002,8(6):1681-1694.
  • 4Knodell RG,Ishak KG,Black WC,et al.Formalation and application of a Numercal scoring system for assessing histological activity in asymptomatic chronic active hepatitis.Hepatology,1981,1(5):431-435.
  • 5MochizukiK,Hayashi N,Hiramatsu N,et al.Fas antigen expression in liver tissues of patients with chronic hepatitis B.JHepatol,1996,24(1):1-7.
  • 6Tsujimoto Y.Bcl-2 family of proteins-Life-or-death switch Clin.Immunol,2001,36(2):266-273.
  • 7Adrain C,Martin SJ.The mitochondrial apoptosome:a killer unleashed by the cytochrome seas.Trends Biochem Sci,2001,26(6):390-397.
  • 8Capaldi RA.The changing face of mitochondrial research.Trends Biochem Sci,2000,25(5):212-214.
  • 9Feldmann G,Haouzi D,Moreau A,et al.Opening of the mitochondrial permeability transition pore causes matrix expansion and outer membrane rupture in Fas-mediated hepatic apoptosis in mice.Hepatology,2000,31(3):674-682.
  • 10Jaeschke H,Bajt ML.Regulation of apoptotic signaling pathways in hepatocytes in vivo.Hepatology 2003,37(4):942-945.

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