The tumor microenvironment and its role in promoting tumor growth.
The tumor microenvironment and its role in promoting tumor growth.
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DOI：
10.1038/onc.2008.271
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发表时间：
2008-10-06
期刊：
影响因子：
8
通讯作者：
Whiteside, T. L.
中科院分区：
文献类型：
--
作者：
Whiteside, T. L.
肿瘤微环境是由肿瘤产生的，并以肿瘤诱导的相互作用为主。尽管各种免疫效应细胞被招募到肿瘤部位，但它们的抗肿瘤功能被下调，这主要是对肿瘤衍生信号的反应。人类肿瘤中存在的炎症细胞浸润本质上是慢性的，并且富含调节性 T 细胞 (Treg) 以及骨髓抑制细胞 (MSC)。肿瘤微环境中的免疫细胞不仅不能发挥抗肿瘤效应功能，反而被选择促进肿瘤生长。肿瘤环境中 NF-κB 通路的持续激活代表了一种似乎有利于肿瘤存活并驱动免疫细胞激活失败的机制。结果是肿瘤逃离宿主免疫系统。肿瘤逃逸是通过激活一种或多种分子机制来实现的，这些机制导致免疫细胞功能的抑制或抗肿瘤效应细胞的凋亡。阻止肿瘤逃逸的能力取决于对肿瘤微环境中运作的细胞和分子途径的更好理解。出现的新治疗策略旨在将促肿瘤微环境改变为有利于急性反应和有效抗肿瘤活性的环境。
The tumor microenvironment is created by the tumor and dominated by tumor-induced interactions. Although various immune effector cells are recruited to the tumor site, their anti-tumor functions are downregulated, largely in response to tumor-derived signals. Infiltrates of inflammatory cells present in human tumors are chronic in nature and are enriched in regulatory T cells (Treg) as well as myeloid suppressor cells (MSC). Immune cells in the tumor microenvironment not only fail to exercise anti-tumor effector functions, but they are co-opted to promote tumor growth. Sustained activation of the NF-κB pathway in the tumor milieu represents one mechanism that appears to favor tumor survival and drive abortive activation of immune cells. The result is tumor escape from the host immune system. Tumor escape is accomplished through the activation of one or several molecular mechanisms that lead to inhibition of immune cell functions or to apoptosis of anti-tumor effector cells. The ability to block tumor escape depends on a better understanding of cellular and molecular pathways operating in the tumor microenvironment. Novel therapeutic strategies that emerge are designed to change the pro-tumor microenvironment to one favoring acute responses and potent anti-tumor activity.
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影响因子：
4.4
作者：
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通讯作者：
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影响因子：
11.2
作者：
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通讯作者：
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影响因子：
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作者：
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影响因子：
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作者：
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通讯作者：
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DOI：
10.1073/pnas.90.8.3539
发表时间：
1993-04-15
影响因子：
11.1
作者：
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通讯作者：
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