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多发性骨髓瘤骨髓组织中p53与血管新生的关系 被引量:1

Correlation of p53 expression and angiogenesis in bone marrow biopsies of multiple myeloma
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摘要 目的 研究多发性骨髓瘤骨髓组织中 p5 3基因和VEGF表达与血管新生的关系。 方法 应用原位杂交及免疫组化染色技术对 4 2例多发性骨髓瘤患者骨髓组织中VEGF、p5 3及微血管密度 (MVD)进行检测。结果 VEGF的阳性率为 5 2 .4 % (2 2 /4 2 ) ,p5 3的阳性率为2 1.4 % (9/4 2 )。经连续切片对比及统计学分析显示 ,p5 3的表达与VEGF的表达显著相关 (P <0 .0 5 ) ;并且p5 3阳性组MVD显著高于阴性组MVD(P <0 .0 1) ,VEGF阳性组MVD显著高于阴性组MVD(P <0 .0 1)。结论 多发性骨髓瘤骨髓组织中 p5 3突变可以上调VEGF的表达 ,促进血管新生。 Objective To investigate the relationship among the expression of p53、vascular endothelial growth factor(VEGF) and angiogenesis in bone marrow biopsies of multiple myeloma.Methods The expression of VEGF、p53 and microvascular density(MVD) were examined by situ hybridization and immunohistochemical staining in bone marrow biopsies of 42 multiple myeloma patients.Results The positive expression rate of VEGF was 52.4%(22/42),the positive expression rate of p53 was 21.4%(9/42).Comparative study of the series sections and statistical analysis revealed that p53 expression was correlated with VEGF(P< 0.05).MVD in p53 positive expression cases was significantly higher than MVD in passive cases(P< 0.01),and MVD in VEGF positive expression cases was significantly higher than MVD in passive cases (P< 0.01).Conclusion The mutant p53 might stimulate angiogenesis by upregulating VEGF expression in bone marrow of multiple myeloma.
出处 《肿瘤防治研究》 CAS CSCD 2003年第6期478-479,共2页 Cancer Research on Prevention and Treatment
关键词 多发性骨髓瘤 骨髓组织 P53 血管新生 原位杂交 免疫组化染色技术 Multiple myeloma p53 VEGF Angiogenesis
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  • 1De Bont ES,Neefjes VME,Rosati S,et al. New vessel formation and aberrant VEGF/VEGFR signaling in acute leukemia:Does it matter [J]. Leuke Lymph,2002,43(10) : 1901-1909.
  • 2Tanaka Y, Abe M, Hiasa M, et al. Myeloma cell-osteoclast interaction enhances angiogenesis together with boneresorption: a role for vascular endothelial cell growth factor and osteopontin[J]. Clin Cancer Res,2007,13(3 ) :816-823.
  • 3Mirshahi P,Toprak SK, Faussat AM, et al. Malignant hematopoietic cells induce an increased expression of VEGFR-1 andVEGFR-3 on bone marrow endothelial cells via AKT and roTOR signalling pathways [J]. Biochem Biophys Res Commun, 2006,349 ( 3 ) : 1003- 1010.

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