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乳腺癌浸润性癌中的血管生成与炎症

Angiogenesis and inflammation in invasive carcinoma of the breast.

作者信息

Lee A H, Happerfield L C, Bobrow L G, Millis R R

机构信息

Hedley Atkins Pathology Laboratory, Guy's Hospital, London, UK.

出版信息

J Clin Pathol. 1997 Aug;50(8):669-73. doi: 10.1136/jcp.50.8.669.

Abstract

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 (x 400 magnification, field 0.168 mm2). 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 rs = 0.17, p = 0.08), and was inversely related to perilobular inflammation (rs = -0.23, p = 0.03).

CONCLUSIONS

The correlations between inflammation and vascularity were weak in this study (r2 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.

摘要

目的

研究乳腺浸润性癌中血管生成与炎症之间的关系。

方法

对75例乳腺浸润性癌切片进行免疫组织化学染色,检测血管性血友病因子、CD3、CD8、CD45RO、CD45RA、CD20、CD68和c-erbB-2。通过计数三个血管最丰富区域的血管数量并计算平均值来评估肿瘤血管生成情况(放大400倍,视野面积0.168平方毫米)。对每种炎症模式进行半定量评分。

结果

主要炎症模式为巨噬细胞弥漫性浸润,T细胞浸润程度较轻。在癌边缘可见血管周围和小叶周围的B细胞和T细胞簇,但不如弥漫性炎症明显。弥漫性炎症,尤其是巨噬细胞,与高肿瘤分级、肿瘤坏死、肿瘤体积大及c-erbB-2表达相关。血管周围和小叶周围炎症也随肿瘤分级增加而增多。肿瘤血管生成随弥漫性炎症强度略有增加(Spearman等级相关系数rs = 0.17,p = 0.08),与小叶周围炎症呈负相关(rs = -0.23,p = 0.03)。

结论

本研究中炎症与血管生成之间的相关性较弱(r2约为0.04),因此没有证据表明存在重要关联。本研究与其他研究之间的差异可能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生成的关系来解决。

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