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》2007年第17期1914-1920,共7页World Chinese Journal of Digestology
基 金:国家自然科学基金;No 30672058
摘 要:目的:探讨树突状细胞(dendritic cells,DCs)浸润对胃癌生物学行为的影响,并探讨DCs浸润程度与肿瘤血管生成的相关性.方法:采用免疫组织化学染色SP法检测胃原发癌35例及其中淋巴转移癌23例组织中S-100^+DCs的密度,同法检测35例胃原发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:随着胃癌浸润程度的增加,间质S-100^+DCs密度的下降,浆膜浸润的胃癌S-100^+DCs密度显著下降,S-100^+DCs与肿瘤浸润深度呈显著负相关(P=0.023);有淋巴转移胃癌S-100^+DCs密度明显低于无淋巴转移者,但无统计学意义;在胃癌转移的淋巴结.随着胃癌转移程度的增加,S-100^+DCs密度显著下降,两者呈显著负相关(r=-0.923,P<0.01);VEGF阳性表达的胃癌S-100^+DCs密度明显低于VEGF阴性表达的胃癌(P=0.157),两者呈负相关(r=-0.128,P=0.464),但均无统计学意义;S-100^+DCs低密度胃癌的MVD显著高于S-100^+DCs高密度胃癌(P=0.013);高MVD胃癌S-100^+DCs密度明显低于低MVD胃癌,胃癌MVD与S-100^+DCs密度呈显著负相关(r= -0.322,P=0.059).结论:胃癌组织的S-100^+DCs浸润程度与胃癌侵袭和淋巴转移密切相关;胃癌DCs浸润程度与肿瘤血管生成的活力密切相关,胃癌细胞释放的VEGF等促血管生成因子可能是肿瘤源性免疫逃逸的重要分子机制之一.AIM: To investigate the potential role of infiltrating dendritic cells (DCs) in the biological behavior of gastric cancer and any association with tumor angiogenesis. METHODS: Immunohistological identification of DCs in gastric cancer using monoclonal antibody recognizing S-100 protein was undertaken in 35 primary gastric cancers (PGC) and 23 lymphoid metastatic gastric cancers (LMGC). Antibodies recognizing vascular endothelial growth factor (VEGF) and CD34 were employed to detect VEGF expression and microvascular density (MVD), respectively. RESULTS: The density of S-100^+DCs was obviously decreased along with progressive cancer invasion of the gastric wall; a statistically significant decrease was seen in gastric cancer with serosal invasion (P = 0,04). Further, a sta- tistically negative correlation between the density of S-100^+DCs and the degree of invasion was shown in gastric cancer (P = 0,023). The density of S-100^+DCs in PGC with lymphatic metastasis was clearly lower than that in PGC with no lymphatic metastasis, though this difference was not statistically significant. How- ever, the density of S-100+DCs in lymph nodes with carcinomatosis showed a marked decrease corresponding to the increase in the percentage of metastasis; a significantly negative correla- tion was shown between them (r = -0.923, P 〈 0.01). The density of S-100^+DCs in VEGF-posi- tive PGC was lower than that in VEGF-negative PGC (P = 0.157). There was a negative association of the density of S-100^+DCs with VEGF expression in PGC, but it was not statistically significant (r = -0.128, P = 0.464). MVD in PGC with lower infiltration of S-100+DCs was significantly higher than that in PGC with higher infiltration (P = 0.013). Similarly, the density of S-100^+DCs in PGC with higher MVD was also lower than that in PGC with lower MVD, thus showing a significantly negative association of the density of S-100~DCs with MVD (r = -0.322, V = 0.059). CONCLUSION: Biological
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