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Research Paper|Volume 14, Issue 6|pp 2720—2735

Tumor-associated macrophages related signature in glioma

Lin-Jian Wang1,2,3, Yimeng Xue2, Yongli Lou3
  • 1Advanced Medical Research Center of Zhengzhou University, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China
  • 2Savaid Medical School, University of Chinese Academy of Sciences, Beijing 100049, China
  • 3Department of Neurosurgery, Zhengzhou Central Hospital Affiliated to Zhengzhou University, Zhengzhou 450007, China
* Equal contribution
Received: December 13, 2021Accepted: March 14, 2022Published: March 24, 2022

Copyright: © 2022 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Background: Glioma is the most common malignant primary tumor with a poor prognosis. Infiltration of tumor-associated macrophages (TAMs) is a hallmark of glioma. However, the regulatory mechanism of TAMs and the prognostic value of related signature in glioma remain unclear.

Methods: TAMs were analyzed by EPIC, MCPCOUNTER and XCELL methods in multiple cohorts, including the TCGA merged GBMLGG, CGGA mRNAseq-325, and CGGA mRNAseq-693. Weighted correlation network analysis (WGCNA) were performed to identify candidate hub genes that might be related to TAMs. The prognostic genes were selected by Univariate Cox regression, Kaplan-Meier analysis and the least absolute shrinkage and selection operator (LASSO) multivariate Cox regression algorithm, and were used to construct a high efficacy prediction model.

Results: Compared with LGG, TAMs of GBM in the TCGA merged GBMLGG, CGGA mRNAseq-693, and CGGA mRNAseq-325 cohorts were increased, and high TAMs levels predicted poorer overall survival for gliomas. The prediction model constructed by nine prognostic genes was highly efficient. The TAMs related risk-score was an independent risk factor for glioma. Moreover, high risk score was correlated with an increased population of TAMs in glioma, as well as the high immune scores, stromal scores and ESTIMATE scores.

Conclusions: Increased TAMs might be an immune evasion mechanism of glioma. In addition, our findings suggested that TAMs-related signature was a valuable prognostic biomarker in glioma and provided therapeutic targets for glioma.