期刊
CANCER CELL
卷 32, 期 1, 页码 42-+出版社
CELL PRESS
DOI: 10.1016/j.ccell.2017.06.003
关键词
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资金
- NIH [P50 CA127001, R01 CA190121, P50 CA097257, RO1 CA120813]
- Cancer Center Support [P30CA16672, P30CA034196]
- Cancer Prevention & Research Institute of Texas (CPRIT) [R140606]
- University Cancer Foundation via the Institutional Research Grant program at the University of Texas MD Anderson Cancer Center
- National Brain Tumor Society Defeat GBM project
- National Brain Tumor Society Oligo Research Fund
- Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI)
- Ministry of Health & Welfare, Republic of Korea [HI14C3418]
- Seve Ballesteros Foundation
- CPRIT [RP140612]
- American Cancer Society [RSG1514501CDD]
- Korea Health Promotion Institute [HI14C3418980017] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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.
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