13073_2023_1175_MOESM1_ESM.docx (19.85 MB)
Additional file 1 of Stalled oligodendrocyte differentiation in IDH-mutant gliomas
journal contribution
posted on 2023-04-14, 03:32 authored by Yanfei Wei, Guanzhang Li, Jing Feng, Fan Wu, Zheng Zhao, Zhaoshi Bao, Wei Zhang, Xiaodong Su, Jiuyi Li, Xueling Qi, Zejun Duan, Yunqiu Zhang, Sandra Ferreyra Vega, Asgeir Store Jakola, Yingyu Sun, Helena Carén, Tao Jiang, Xiaolong FanAdditional file 1: Fig. S1. Differential transcriptomic and mutational profiles in PM gliomas with or without 1p19q co-deletion. Fig. S2. Declining expression of NFOL and MFOL signatures in PM gliomas from GSE4290. Fig. S3. Declining expression of NFOL and MFOL signatures in PM gliomas from the REMBRANDT dataset. Fig. S4. Genes upregulated in the PM gliomas were enriched in murine OPCs. Fig. S5. Genes concordantly enriched in both PM subtypes were differentially expressed between OPC and MO, but not between developing astrocyte and mature astrocyte. Fig. S6. Enrichment of gene ontology terms in genes concordantly upregulated in the PM gliomas as shown in Fig. 1C. Fig. S7. Suppressed myelination program in PM gliomas from GSE4290. Fig. S8. No distinct expression of astrocytic lineage genes between PM gliomas and NT brain tissues. Fig. S9. Co-staining of LFB and hematoxylin-eosin of representative IDH-WT GBMs. Fig. S10. Uniform expression of early oligodendrocytic lineage markers in individual PM glioma cells from additional samples. Fig. S11. Enriched expression of previously reported oligodendrocytic (OC) lineage signature and astrocytic (AC) lineage signature in O/C1 and O/C2 cell populations, respectively. Fig. S12. Sporadic or heterogeneous expression of OPC and COP markers in individual EM glioma cells. Fig. S13. Expression of OPC and COP markers in individual PM glioma cells validated with RNAscope analysis. Fig. S14. EM and PM gliomas show marked difference in cell proliferation as assessed with Ki-67 staining in clinical samples. Fig. S15. OPCs and COPs in juvenile and adult brain are sporadically in cell cycle. Fig. S16. Proliferating and non-proliferating IDH-mutant glioma cells are similar at the global transcriptome level. Fig. S17. Top 70 genes with most significant CpGs in IDH-wildtype GBMs. Fig. S18. Myelination profiles of myelination regulator, hallmarks of MO and regulators of OPC specification and maintenance in PM gliomas.
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National Natural Science Foundation of China Key Technologies Research and Development Program VINNOVA
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substantiated using datacommon developmental hierarchyaccommodate biological featuresproliferating cells resemblecommitted oligodendrocyte progenitorsrecent studies reportoligodendrocyte progenitor cellsblocked myelination programmutant glioma cellswithout 1p19q cooligodendrocyte differentiation dueseq data demonstrategene expression profilesoligodendrocyte lineage differentiationmutant gliomas shareoligodendrocyte lineage stageharboring 1p19q coastrocyte lineage markersstalled oligodendrocyte differentiationidentified genes enrichedoligodendrocyte lineage1p19q comyelinating oligodendrocytemutant gliomasstudies showmyelination regulatorsastrocyte precursorsdifferentiation stagesdifferentiation stagequiescent cellswhereas regulatorstherapy developmentspecific markersneural lineageskey regulatorsgenomic alterationsforming oligodendrocytesfindings provideexpression patternearly stagesdna methylationdespite differencesclinical manifestationclassification guidelinecell transcriptomescell atac
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