国家神经系统疾病临床医学研究中心数据管理与共享系统

Data Management And Sharing System of China National Clinical Research Center for Neurological Diseases

Genetic and clinical characterization of B7-H3 (CD276) expression and epigenetic regulation in diffuse brain glioma

第一作者:Wang Zhiliang

通讯作者:Jiang Tao

B7-H3 checkpoint inhibitors glioma immune response

基本信息

  • 负责人:Wang Zhiliang
  • 数据来源: OTHERS
  • 论文编号:OTHERS20190626
  • 发表时间:2018-09-01

2018-09-01

已发表文章

发表杂志:Cancer Sci

发表类型: Research Article

影响因子(IF): 6.716

PMID: 30027617 Pubmed原文链接 全文下载

主要研究背景及目的

方法

We set out to characterize the expression pattern and biological function of B7-H3 in brain gliomas using high-throughput data obtained from the Chinese Glioma Genome Atlas (CGGA) and the Cancer Genome Atlas (TCGA) projects. B7-H3 was upregulated more in higher-grade gliomas than that in lower-grade gliomas in both CGGA and TCGA datasets. Isocitrate dehydrogenase (IDH) mutation seemed to exert significant influence on B7-H3 expression in gliomas but led to quite different results between grade II gliomas and higher-grade gliomas. In addition to IDH, methylation of B7-H3 promoter and microRNA-29 family also showed a potential regulatory effect on B7-H3 expression. Gene ontology analysis revealed that B7-H3 was associated with mitotic cell cycle, cell proliferation and immune response.

结论

Higher B7-H3 expression indicates a worse prognosis for glioma patients, which warrants further research into the development of inhibitors for targeting this immune checkpoint, but we still need to be cautious about immune checkpoint inhibition for central nervous system tumors.

主要结果

Further investigation suggested that B7-H3 was mostly involved in the Toll-like receptor signaling pathway. Survival analysis indicated that B7-H3 was an independent unfavorable prognosticator for glioma patients in both CGGA and TCGA datasets. B7-H3 expression is regulated by multiple mechanisms and is potentially involved in the T-cell receptor signaling pathway.