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1. Integrated molecular and multiparametric MRI mapping of high-grade glioma identifies regional biologic signatures

2. Regulated interaction of ID2 with the anaphase-promoting complex links progression through mitosis with reactivation of cell-type-specific transcription

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3. Single-cell characterization of macrophages in glioblastoma reveals MARCO as a mesenchymal pro-tumor marker

4. Anti-tumor effects of an ID antagonist with no observed acquired resistance

5. Tissue-specific modifier alleles determine Mertk loss-of-function traits

6. De novo gene signature identification from single‐cell RNA‐seq with hierarchical Poisson factorization

7. Single-cell transcriptome analysis of lineage diversity in high-grade glioma

8. A recurrent point mutation in PRKCA is a hallmark of chordoid gliomas

9. A Small-Molecule Pan-Id Antagonist Inhibits Pathologic Ocular Neovascularization

10. HUWE1 is a critical colonic tumour suppressor gene that prevents MYC signalling, DNA damage accumulation and tumour initiation

11. LZTR1Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL

12. Supplementary Figure S5 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL

13. Data from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL

14. Supplementary Tables S1-S3 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL

15. Table S2 from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma

16. Data from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma

17. Supplementary Data from Cross-Cohort Analysis Identifies a TEAD4–MYCN Positive Feedback Loop as the Core Regulatory Element of High-Risk Neuroblastoma

19. Data from Novel SEC61G–EGFR Fusion Gene in Pediatric Ependymomas Discovered by Clonal Expansion of Stem Cells in Absence of Exogenous Mitogens

20. Supplementary Figure 4 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

21. Supplementary Figure 3 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

22. Supplementary Figure 2 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

23. Supplementary Figure Legends from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

24. Supplementary Table 1 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

25. Supplementary Table S1 from Novel SEC61G–EGFR Fusion Gene in Pediatric Ependymomas Discovered by Clonal Expansion of Stem Cells in Absence of Exogenous Mitogens

26. Supplementary Figure 6 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

27. Supplementary Figures from Huwe1 Sustains Normal Ovarian Epithelial Cell Transformation and Tumor Growth through the Histone H1.3-H19 Cascade

28. Data from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

29. Supplementary Figure 1 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

30. Data from Huwe1 Sustains Normal Ovarian Epithelial Cell Transformation and Tumor Growth through the Histone H1.3-H19 Cascade

31. Supplementary Materials and Methods from Novel SEC61G–EGFR Fusion Gene in Pediatric Ependymomas Discovered by Clonal Expansion of Stem Cells in Absence of Exogenous Mitogens

32. Figures S1, S2, S3, S4, S5, and S6 from Novel SEC61G–EGFR Fusion Gene in Pediatric Ependymomas Discovered by Clonal Expansion of Stem Cells in Absence of Exogenous Mitogens

33. Supplementary Figure 5 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma

34. Supplemental Methods and References,Supplementary Figures S1-S3, and Supplementary Table S1 from RHPN2 Drives Mesenchymal Transformation in Malignant Glioma by Triggering RhoA Activation

37. Integrative multi-omics networks identify PKCδ and DNA-PK as master kinases of glioblastoma subtypes and guide targeted cancer therapy

39. Glioma progression is shaped by genetic evolution and microenvironment interactions

40. Tissue-specific modifier alleles determineMertkloss-of-function traits

41. Abstract 1507: Multiregional sampling of high grade glioma identifies regional biologic signatures

42. Abstract 5621: Multi-parametric MRI maps regional heterogeneity of high grade glioma phenotypes

43. EPCO-27. REVEALING TUMOR HETEROGENEITY AND IMMUNE MICROENVIRONMENT IN NF-1 GLIOMA BY SINGLE-CELL GENE EXPRESSION PROFILING

45. Inhibition of ERK/MAPK signaling as potential therapy to prevent optic pathway glioma in infants with neurofibromatosis type 1

46. CSIG-01. EGFR AND AXL RECEPTOR TYROSINE KINASES DRIVE ONCOGENESIS BY LZTR1 MUTATION

47. EPCO-05. DIFFERENTIAL MOLECULAR PROFILING OF IDH WILD TYPE GLIOBLASTOMA SURVIVORS REVEALS THE ASSOCIATION OF NEOANTIGEN QUALITY WITH EXCEPTIONAL LONG SURVIVAL

48. EXTH-21. DEVELOPMENT OF THERAPEUTIC STRATEGIES BY PATHWAY-BASED MULTI-OMICS APPROACH AND MASTER KINASE ANALYSIS IN GLIOBLASTOMA MULTIFORME

49. EPCO-03. PATHWAY-BASED STRATIFICATION OF GLIOBLASTOMA BY MULTI-OMICS INFORMS SUBTYPE-SPECIFIC MASTER KINASES-PHOSPHOSITE SUBSTRATES

50. The epigenetic evolution of gliomas is determined by their IDH1 mutation status and treatment regimen