Tumor evolution of glioma intrinsic gene expression subtype associates with immunological changes in the microenvironment
By Qianghu Wang, Baoli Hu, Xin Hu, Hoon Kim, M. Squatrito, L. Scarpace, A. deCarvalho, Sali Lyu, Pengping Li, Yan Li and 24 more. Cancer Cell, 2017
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Summary We leveraged IDH wild-type glioblastomas, derivative neurospheres, and single cell gene expression profiles to define three tumor-intrinsic transcriptional subtypes designated as proneural, mesenchymal, and classical. Transcriptomic subtype multiplicity correlated with increased intratumoral heterogeneity and presence of tumor microenvironment. In silico cell sorting identified macrophages/microglia, CD4+ T lymphocytes, and neutrophils in the glioma microenvironment. NF1 deficiency resulted in increased tumor-associated macrophages/microglia infiltration. Longitudinal transcriptome analysis showed that expression subtype is retained in 55% of cases. Gene signature-based tumor microenvironment inference revealed a decrease in invading monocytes and a subtype-dependent increase in macrophages/microglia cells upon disease recurrence. Hypermutation at diagnosis or at recurrence associated with CD8+ T cell enrichment. Frequency of M2 macrophages detection associated with short-term relapse after radiation therapy.
Subfields: Genetics, Immunology, Neurology
View Paper: https://www.semanticscholar.org/paper/fbfb05b467b2c6ae80c894a835eaeefe5e1dd6c4
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Citations in the corpus
- Chinese Glioma Genome Atlas (CGGA): A Comprehensive Resource with Functional Genomic Data from Chinese Glioma Patients (2021, background): “Glioma recurrence or malignant progression occurs likely for several reasons: (1) infiltrative tumor cells cannot be completely removed by neurosurgical resection [9,10]; (2) residual tumor cells cannot be effectively suppressed by limited postoperative treatment options [3,11,12]; (3) multiple lesi”
- An integrative model of cellular states, plasticity and genetics for glioblastoma (2019, positive): “Similarly, the TCGA-MES subtype corresponds to a combination of the MES-like malignant state defined above and a preponderance of microglia and macrophages (Figure S5C), supporting ), and proliferation (Ki67) markers.”