Core Needle Biopsy Enhances the Activity of the CCL2/CCR2 Pathway in the Microenvironment of Invasive Breast Cancer

Onco Pub Date : 2021-12-30 DOI:10.3390/onco2010001
M. Heiskala, K. Joensuu, P. Heikkilä
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引用次数: 1

Abstract

The use of core needle biopsy (CNB) as a means to verify malignancy preoperatively is a paradigm in current breast cancer care, and the risk of enhancing tumor development by this procedure has been considered insignificant. Experimental work in mice has shown preoperative biopsies to increase tumor supportive elements in the microenvironment, whereas, in humans, the impact of CNB on the host’s immunologic response has not been investigated. In this pilot study, we compared the expression of CCL2/CCR2 pathway components at the protein level in samples from CNBs to those from the corresponding resected tumors from 52 patients with primary breast cancer. We found an increased expression of CD163, CD14 and CCR2 in monocytes/macrophages and a slight decrease of CCL2 in the malignant epithelium in the tumors after the biopsy. The increased infiltration of immunosuppressive monocytes/macrophages and the decreased tumor cell CCL2 expression, presumably due to the CCR2 availability-dependent CCL2 internalization, suggest that CNB enhances the activity of the CCL2/CCR2 pathway, and this finding warrants confirmatory examination. The switch in the context-dependent role of CCL2 on the polarization of macrophages may lead to increased tumor supportive function both locally and in the peripheral immune machinery. The future directions in breast cancer should include early interventions to support the tumor surveillance of the host.
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核针穿刺增强侵袭性乳腺癌症微环境中CCL2/CCR2通路的活性
使用核心针活组织检查(CNB)作为术前验证恶性程度的手段是当前癌症治疗的一种模式,这种方法增强肿瘤发展的风险被认为是微不足道的。在小鼠身上的实验工作表明,术前活检可以增加微环境中的肿瘤支持元素,而在人类身上,CNB对宿主免疫反应的影响尚未得到研究。在这项初步研究中,我们比较了CNB样品与52例原发性癌症患者相应切除肿瘤样品中CCL2/CCR2途径成分在蛋白质水平上的表达。活检后,我们发现单核细胞/巨噬细胞中CD163、CD14和CCR2的表达增加,肿瘤恶性上皮中CCL2的表达略有下降。免疫抑制单核细胞/巨噬细胞的浸润增加和肿瘤细胞CCL2表达减少,可能是由于CCR2的可用性依赖性CCL2内化,表明CNB增强了CCL2/CCR2途径的活性,这一发现值得验证。CCL2在巨噬细胞极化中的上下文依赖性作用的转变可能导致局部和外周免疫机制中肿瘤支持功能的增加。癌症的未来方向应包括早期干预,以支持宿主的肿瘤监测。
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