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有和没有贝伐珠单抗治疗的人透明细胞肾细胞癌中的微血管密度、巨噬细胞和肥大细胞。

Microvascular density, macrophages, and mast cells in human clear cell renal carcinoma with and without bevacizumab treatment.

机构信息

Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Bari, Italy.

Department of Emergency and Organ Transplantation-Urology, Andrology and Kidney Transplantation Unit, University of Bari Medical School, Bari, Italy.

出版信息

Urol Oncol. 2019 Jun;37(6):355.e11-355.e19. doi: 10.1016/j.urolonc.2019.01.025. Epub 2019 Feb 6.

DOI:10.1016/j.urolonc.2019.01.025
PMID:30738745
Abstract

BACKGROUND

Clear cell renal cell carcinoma (ccRCC) represents a highly vascularized aggressive kidney cancer. Due to ccRCC chemotherapy resistance, antiangiogenesis is one of the most innovative targeted therapies for this tumor. The tumor microenvironment exerts important roles in tumor growth, angiogenesis, and metastatic escape.

MATERIALS AND METHODS

In this study, we investigated the composition of tumor cell microenvironment including mast cells, macrophages, and microvascular density in ccRCC tumor tissues collected from patients who underwent nephrectomy treated or not with bevacizumab as neoadjuvant therapy before surgery.

RESULTS

The results of this study indicate that bevacizumab-treated ccRCC samples present reduced microvascular density as well as a lower number of CD68-positive macrophages and tryptase-positive mast cells in comparison with the untreated patients.

CONCLUSIONS

It follows that the antiangiogenic activity of bevacizumab may be due to a direct effect on angiogenic cytokines released by tumor cells and an indirect effect on the release of pro-angiogenic factors by inflammatory stromal cells.

摘要

背景

透明细胞肾细胞癌(ccRCC)是一种高度血管化的侵袭性肾癌。由于 ccRCC 对化疗的耐药性,抗血管生成是针对该肿瘤最具创新性的靶向治疗之一。肿瘤微环境在肿瘤生长、血管生成和转移逃逸中发挥着重要作用。

材料和方法

在这项研究中,我们研究了包括肥大细胞、巨噬细胞和微血管密度在内的肿瘤细胞微环境的组成,这些肿瘤细胞取自接受或未接受贝伐珠单抗作为新辅助治疗的肾切除术患者的 ccRCC 肿瘤组织。

结果

与未治疗的患者相比,贝伐珠单抗治疗的 ccRCC 样本中的微血管密度降低,并且 CD68 阳性巨噬细胞和类胰蛋白酶阳性肥大细胞的数量减少。

结论

贝伐珠单抗的抗血管生成活性可能是由于其对肿瘤细胞释放的血管生成细胞因子的直接作用,以及对炎症性基质细胞释放促血管生成因子的间接作用。

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