Cancer Cell-Autonomous Parainflammation Mimics Immune Cell Infiltration.
Cancer Cell-Autonomous Parainflammation Mimics Immune Cell Infiltration.
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DOI：
10.1158/0008-5472.can-16-3383
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发表时间：
2017-07-15
期刊：
影响因子：
11.2
通讯作者：
Ben-Neriah Y
中科院分区：
文献类型：
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作者：
Lasry A;Aran D;Butte AJ;Ben-Neriah Y
副炎症是炎症的一种独特变体，其特征在于上皮自主激活炎症反应。已显示副炎症在p53丧失后强烈促进小鼠肠道肿瘤发生。在最近的一项研究中，我们探讨了人类癌症中副炎症的患病率，并确定了其与影响治疗和预后的某些分子和临床参数的关系。副炎症可以从40个基因标签中鉴定，并且在癌细胞系和多种原发性肿瘤中发现，与肿瘤微环境无关。在这里，我们讨论了我们的研究结果在肿瘤微环境分析中的意义，表明肿瘤细胞基因表达可能经常模仿免疫和炎症浸润，在解释肿瘤表达数据时应谨慎。我们还讨论了特定类型肿瘤中副炎症与p53突变患病率之间的联系，以及定期使用非甾体抗炎药预防癌症。我们认为，副炎症可能作为一种新的生物标志物筛选患者谁可能特别受益于NSAID治疗。
Parainflammation is a unique variant of inflammation, characterized by epithelial-autonomous activation of inflammatory response. Parainflammation has been shown to strongly promote mouse gut tumorigenesis upon p53 loss. In a recent study, we explored the prevalence of parainflammation in human cancer and determined its relationship to certain molecular and clinical parameters affecting treatment and prognosis. Parainflammation can be identified from a 40-gene signature, and is found in both carcinoma cell lines and a variety of primary tumors, independently of tumor microenvironment. Here we discuss the implications of our findings in analyses of tumor microenvironment, suggesting that as tumor cell gene expression may often mimic immune and inflammatory infiltration, caution should be applied when interpreting tumor expression data. We also address the connection between parainflammation and prevalence of p53 mutations in specific types of tumors, and cancer prevention by regular usage of NSAIDs. We suggest that parainflammation may serve as a novel biomarker for screening patients who may particularly benefit from NSAID treatment.