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The relationship between microvessel count and the expression of vascular endothelial growth factor p53 and K-ras in non-small cell lung cancer.

机译:非小细胞肺癌中微血管计数与血管内皮生长因子p53和K-ras表达的关系。

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摘要

Using immunohistochemical staining, we studied the relationship between the microvessel count (MC) and the expression of K-ras, mutant p53 protein, and vascular endothelial growth factor (VEGF) in 61 surgically resected non-small cell lung cancers (NSCLC) (42 squamous cell carcinoma, 14 adenocarcinoma, 2 large cell carcinoma, 2 adenosquamous carcinoma, and 1 mucoepidermoid carcinoma). MC of the tumors with lymph node (LN) metastasis was significantly higher than that of tumors without LN metastasis (66.1+/-23.1 vs. 33.8+/-13.1, p<0.05). VEGF was positive in 54 patients (88.5%). MC was 58.1+/-25.2 (mean+/-S.D.) in a x200 field, and it was significantly higher in VEGF(+) tumors than in VEGF(-) tumors (61.4+/-23.7 vs. 32.9+/-23.8, p<0.05). VEGF expression was higher in K-ras-positive or mutant p53-positive tumors than in negative tumors (p<0.05). MC was significantly higher in K-ras(+) tumors than in K-ras(-) tumors, although it did not differ according to the level of mutant p53 protein expression. Survival did not differ with VEGF, mutant p53, or K-ras expression, or the level of MC. In conclusion, there is a flow of molecular alterations from K-ras and p53, to VEGF expression, leading to angiogenesis and ultimately lymph node metastasis. Correlations between variables in close approximation and the lack of prognostic significance of individual molecular alterations suggest that tumorigenesis and metastasis are multifactorial processes.
机译:我们使用免疫组织化学染色研究了61例手术切除的非小细胞肺癌(NSCLC)中微血管计数(MC)与K-ras,突变型p53蛋白和血管内皮生长因子(VEGF)表达之间的关系(42鳞状细胞癌,14例腺癌,2例大细胞癌,2例腺鳞癌和1例粘液表皮样癌)。有淋巴结转移的肿瘤的MC显着高于无淋巴结转移的肿瘤的MC(66.1 +/- 23.1 vs. 33.8 +/- 13.1,p <0.05)。 VEGF阳性54例(88.5%)。在x200视野中,MC为58.1 +/- 25.2(平均+/- SD),在VEGF(+)肿瘤中明显高于VEGF(-)肿瘤(61.4 +/- 23.7与32.9 +/- 23.8, p <0.05)。在K-ras阳性或突变型p53阳性肿瘤中,VEGF表达高于阴性肿瘤(p <0.05)。 MC在K-ras(+)肿瘤中显着高于K-ras(-)肿瘤,尽管根据突变型p53蛋白表达水平并没有差异。存活率与VEGF,突变体p53或K-ras表达或MC水平无差异。总之,存在从K-ras和p53到VEGF表达的分子变化,导致血管生成和最终的淋巴结转移。变量之间的相关性非常接近,并且各个分子的变化缺乏预后意义,提示肿瘤发生和转移是多因素过程。

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