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肝细胞癌的血管生成:一项免疫组织化学研究。

Angiogenesis of hepatocellular carcinoma: An immunohistochemistry study.

作者信息

Fodor Decebal, Jung Ioan, Turdean Sabin, Satala Catalin, Gurzu Simona

机构信息

Department of Pathology, University of Medicine, Pharmacy, Sciences and Technology, Targu Mures 530149, Romania.

出版信息

World J Hepatol. 2019 Mar 27;11(3):294-304. doi: 10.4254/wjh.v11.i3.294.

DOI:10.4254/wjh.v11.i3.294
PMID:30967907
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6447418/
Abstract

BACKGROUND

Although hepatocellular carcinoma (HCC) is one of the most vascular solid tumors, antiangiogenic therapy has not induced the expected results.

AIM

To uncover immunohistochemical (IHC) aspects of angiogenesis in HCC.

METHODS

A retrospective cohort study was performed and 50 cases of HCC were randomly selected. The angiogenesis particularities were evaluated based on the IHC markers Cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF) A and the endothelial area (EA) was counted using the antibodies CD31 and CD105.

RESULTS

The angiogenic phenotype evaluated with VEGF-A was more expressed in small tumors without vascular invasion (pT1), whereas COX-2 was rather expressed in dedifferentiated tumors developed in non-cirrhotic liver. The CD31-related EA value decreased in parallel with increasing COX-2 intensity but was higher in HCC cases developed in patients with cirrhosis. The CD105-related EA was higher in tumors developed in patients without associated hepatitis.

CONCLUSION

In patients with HCC developed in cirrhosis, the newly formed vessels are rather immature and their genesis is mediated VEGF. In patients with non-cirrhotic liver, COX-2 intensity and number of mature neoformed vessels increases in parallel with HCC dedifferentiation.

摘要

背景

尽管肝细胞癌(HCC)是血管最丰富的实体瘤之一,但抗血管生成治疗并未取得预期效果。

目的

揭示HCC血管生成的免疫组织化学(IHC)特征。

方法

进行一项回顾性队列研究,随机选取50例HCC病例。基于免疫组织化学标志物环氧合酶-2(COX-2)、血管内皮生长因子(VEGF)A评估血管生成特性,并使用抗体CD31和CD105计数内皮面积(EA)。

结果

用VEGF-A评估的血管生成表型在无血管侵犯的小肿瘤(pT1)中表达更明显,而COX-2在非肝硬化肝脏中发生的去分化肿瘤中表达较多。与CD31相关的EA值随COX-2强度增加而降低,但在肝硬化患者发生的HCC病例中更高。与CD105相关的EA在无相关肝炎患者发生的肿瘤中更高。

结论

在肝硬化患者发生的HCC中,新形成的血管相当不成熟,其生成由VEGF介导。在非肝硬化肝脏患者中,COX-2强度和成熟新生血管数量随HCC去分化而增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a10/6447418/6885c9d2f5a8/WJH-11-294-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a10/6447418/c8165ecfc05e/WJH-11-294-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a10/6447418/2c3dea70fa41/WJH-11-294-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a10/6447418/6885c9d2f5a8/WJH-11-294-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a10/6447418/c8165ecfc05e/WJH-11-294-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a10/6447418/2c3dea70fa41/WJH-11-294-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7a10/6447418/6885c9d2f5a8/WJH-11-294-g003.jpg

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