T cell exhaustion methylation signature drives differential immune responses in glioblastoma

Bibliographic Details
Title: T cell exhaustion methylation signature drives differential immune responses in glioblastoma
Authors: Feng Chen, Wen-Bo Qian, Zhen-Hua Chen, Jun Qian, Chun Luo
Source: Discover Oncology, Vol 15, Iss 1, Pp 1-13 (2024)
Publisher Information: Springer, 2024.
Publication Year: 2024
Collection: LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens
Subject Terms: Consensus clustering, Glioblastoma, Survival analysis, T cell exhaustion, TEXM signature, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282
More Details: Abstract Background Methylation-related signatures play crucial roles in tumorigenesis and progression. However, their roles in the immune response in primary glioblastoma (GBM) remains unclear. Methods We analyzed the differential expression of specific members of T cell exhaustion-related pathways in GBM from the perspective of T cell exhaustion. We further screened for significantly negatively correlated methylation sites as candidate methylation markers for T cell exhaustion. Using consensus clustering, we divided the samples into two categories with significant differences in overall survival (OS). We then performed univariate and multivariate Cox regression analyses to construct the T Cell Exhaustion Methylation (TEXM) signature. Finally, we confirmed that this signature served as an independent prognostic factor, and further characterized it in terms of drug resistance and immunotherapy. Results We identified 95 significantly differentially expressed T cell exhaustion-related genes and 51 methylation markers associated with T cell exhaustion. The cancer samples were classified according to methylation site markers, thus indicating two subtypes with significant differences in OS: subtype A and subtype B. Tumor scores, stromal scores, tumor purity, and ESTIMATE scores all showed significant differences between subtypes (P
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2730-6011
Relation: https://doaj.org/toc/2730-6011
DOI: 10.1007/s12672-024-01412-3
Access URL: https://doaj.org/article/ed0068d59fdf4a25a39eba7745a7b341
Accession Number: edsdoj.0068d59fdf4a25a39eba7745a7b341
Database: Directory of Open Access Journals
More Details
ISSN:27306011
DOI:10.1007/s12672-024-01412-3
Published in:Discover Oncology
Language:English