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作 者:周业江[1] 熊玉霞[2] 易国平[1] 徐亮[1] 夏冬[1] 魏仁智[1]
机构地区:[1]泸州医学院附属医院普外科,四川省泸州市646000 [2]泸州医学院药理教研室,四川省泸州市646000
出 处:《世界华人消化杂志》2006年第30期2938-2942,共5页World Chinese Journal of Digestology
基 金:国家自然科学基金资助项目;No.30672058
摘 要:目的:探讨胃癌细胞Granzyme B(GrB)表达在肿瘤血管生成和淋巴转移中的作用.方法:以细胞毒T淋巴细胞为内对照,采用免疫组织化学染色S-P法检测35例胃癌及其中23例淋巴转移癌细胞GrB蛋白的表达;同法检测35例胃癌血管内皮生长因子(VEGF)的表达及CD34标记的微血管密度(MVD).结果:GrB的表达在无淋巴转移的胃癌高于有淋巴转移者,但无显著性差异,但淋巴转移灶的胃癌细胞GrB阳性率较相应的原发肿瘤显著增高(P=0.038);胃癌GrB与VEGF表达的同步率达57.1%,两者表达水平无明显相关性,而GrB表达水平与胃癌MVD呈显著负相关(r=-0.421,P=0.012);GrB阳性胃癌无论其VEGF表达水平如何,其MVD无显著差异; VEGF阳性胃癌MVD与GrB的表达状态明显相关,GrB阳性者MVD显著下降(P=0.023),在VEGF阴性胃癌中也有类似结果;GrB+&VEGF-表型胃癌MVD最低,VEGF+&GrB-表型胃癌MVD最高,两者有显著性的差异(P= 0.013).结论:胃癌细胞GrB表达可能有助于抑制肿瘤血管生成,但也可能有助于淋巴转移胃癌细胞的存活.AIM: To investigate the potential role of Granzyme B (GrB) in the biological behavior of gastric cancer, such as angiogenesis and lymphatic metastasis. METHODS: The identification of GrB expression in gastric cancer cells was performed immunohistologically in patients with primary gastric cancers (PGC, n = 35) and lymphoid metastatic gastric cancer (LMGC, n = 23), and GrB^+ cycotoxic T lymphocytes (CTL) served as positive internal control.The antibodies recognizing vascular endothelial growth factor (VEGF) and CD34 were employed to detect the VEGF expression and microvascular density (MVD), respectively. RESULTS: The positive rate of GrB expression was relatively lower in PGC with lymphoid metastasis than that without metastasis, but no significant difference was observed (P = 0.709). The positive rate of GrB expression in LMGC was significantly higher than that in the corresponding PGC (P = 0.038). The synchronous expression rate of GrB and VEGF came up to 57.1%, while there was no significant correlation between them. A significant negative correlation was found between the level of GrB expression and MVD (r=-0.421, P = 0.012) in PGC. VEGF expression was showed to have no significant effect on MVD in GrB positive PGC (P = 0.494). However, the decreased MVD in VEGF^+ PGC was remarkably associated with GrB expression (P = 0.023), and similar feature was exhibited in VEGF negative PGC (P = 0.134). The lowest and the highest MVD were demonstrated in PGC with positive GrB and negative VEGF, and PGC with positive VEGF and negative GrB, respectively (P = 0.013). CONCLUSION: The over-expression of GrB in gastric cancer cells might contribute to the inhibition of tumor angiogenesis, but also might contribute to the survival potential of diffused tumor cells in lymph gland.
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