Angiogenesis and inflammation in invasive carcinoma of the breast

Angiogenesis and inflammation in invasive carcinoma of the breast
复制标题

DOI:
10.1136/jcp.50.8.669
复制
发表时间:
1997-08-01
影响因子:
3.4
通讯作者:
Millis, RR
Millis, RR
中科院分区:
医学3区
文献类型:
--
作者:
Lee, AHS;Happerfield, LC;Millis, RR

文献摘要

被引文献

相似文献

目的:探讨乳腺浸润性癌组织中血管生成与炎症的关系。方法采用免疫组织化学方法检测75例乳腺浸润性癌组织中von Willebrand因子、CD3、CD8、CD45RO、CD45RA、CD20、CD68和c-erbB-2的表达。通过计数血管最多的三个区域的血管,并计算平均值(x400放大倍数,视野0.168 mm(2))来评估肿瘤的血管。结果:炎症的主要类型是巨噬细胞的弥漫性渗透,其次是T细胞。癌边缘可见血管周围和小叶周围的B、T细胞团,但不明显于弥漫性炎症。弥漫性炎症,特别是巨噬细胞,与高级别肿瘤、肿瘤坏死、肿瘤大小和c-erbB-2表达有关。血管周围和小叶周围炎症也随着肿瘤分级的增加而增加。肿瘤血管密度随弥漫性炎症程度的加重而轻微增加(S等级相关系数r(S)=0.17,p=0.08),与小叶周围炎症程度呈负相关(r(S)=-0.23,p=0.03)。结论:炎症与肿瘤血管密度的相关性较弱(r(2)约0.04),因此尚无重要相关性的证据。这项研究与其他研究之间的差异可以通过研究肿瘤浸润性炎症细胞中血管生成细胞因子和蛋白水解酶的表达及其与肿瘤血管的关系来解决。
Aim-To investigate the relation between angiogenesis and inflammation in invasive carcinoma of the breast.Methods-Sections from 75 invasive carcinomas of the breast were stained using immunohistochemistry for von Willebrand factor, CD3, CD8, CD45RO, CD45RA, CD20, CD68, and c-erbB-2. Tumour vascularity was assessed by counting vessels in the three most vascular areas, and calculating the average (x400 magnification, field 0.168 mm(2)). Each pattern of inflammation was scored semiquantitatively.Results-The main pattern of inflammation was a diffuse infiltrate of macrophages, and to a lesser extent T cells. Perivascular and perilobular clusters of B and T cells were noted at the edge of the carcinomas, but were less prominent than the diffuse inflammation. Diffuse inflammation, particularly macrophages, was associated with high tumour grade, tumour necrosis, large tumour size, and c-erbB-2 expression. Perivascular and perilobular inflammation also increased with tumour grade. Tumour vascularity increased slightly with intensity of diffuse inflammation (Spearman's rank correlation coefficient r(s) = 0.17, p = 0.08), and was inversely related to perilobular inflammation (r(s) = -0.23, p = 0.03).Conclusions-The correlations between inflammation and vascularity were weak in this study (r(2) about 0.04) and thus there was no evidence of an important relation. Discrepancies between this and other studies may be resolved by studying expression of angiogenic cytokines and proteolytic enzymes by tumour infiltrating inflammatory cells, and their relation to tumour vascularity.