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2. Targeting integrated epigenetic and metabolic pathways in lethal childhood PFA ependymomas

4. Human fetal cerebellar cell atlas informs medulloblastoma origin and oncogenesis

5. The NALCN channel regulates metastasis and nonmalignant cell dissemination

6. Author Correction: Cancer-associated DDX3X mutations drive stress granule assembly and impair global translation

7. Spectrum and prevalence of genetic predisposition in medulloblastoma: a retrospective genetic study and prospective validation in a clinical trial cohort.

8. Natural language processing charts transcriptome evolution to design combination cancer therapies

10. Vismodegib Exerts Targeted Efficacy Against Recurrent Sonic Hedgehog–Subgroup Medulloblastoma: Results From Phase II Pediatric Brain Tumor Consortium Studies PBTC-025B and PBTC-032

13. DDX3X acts as a live-or-die checkpoint in stressed cells by regulating NLRP3 inflammasome

14. Challenges to curing primary brain tumours

17. Primary cilia control translation and the cell cycle in medulloblastoma

18. Data from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

19. Table S2 from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

20. Figure S2 from ZFTA–RELA Dictates Oncogenic Transcriptional Programs to Drive Aggressive Supratentorial Ependymoma

21. Table S2 from ZFTA–RELA Dictates Oncogenic Transcriptional Programs to Drive Aggressive Supratentorial Ependymoma

22. Data from ZFTA–RELA Dictates Oncogenic Transcriptional Programs to Drive Aggressive Supratentorial Ependymoma

23. Supplementary Table S4 from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

24. Data from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

25. Figure S2 from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

26. Supplementary Methods from ZFTA Translocations Constitute Ependymoma Chromatin Remodeling and Transcription Factors

27. Supplementary Data from Cross-Species Genomics Reveals Oncogenic Dependencies in ZFTA/C11orf95 Fusion–Positive Supratentorial Ependymomas

28. Supplementary Fig 5 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

29. Supplementary Figure Legends from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

30. Supplementary Figure Legends 1-3 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

31. Figure S4 from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

32. Appendix from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

33. Supplementary Fig 1 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

34. Supplementary Tables 1 - 3 from Phase I Study of Vismodegib in Children with Recurrent or Refractory Medulloblastoma: A Pediatric Brain Tumor Consortium Study

35. Supplementary Figure 3 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

36. supplemental figure and table legend from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

37. Supplementary Fig 2 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

38. Supplementary Fig 7 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

39. Supplementary Fig 3 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

40. Supplementary Data from Rapid Diagnosis of Medulloblastoma Molecular Subgroups

41. Figure S1 from Establishing a Preclinical Multidisciplinary Board for Brain Tumors

42. Table S1-S3 from Molecular Characterization of Choroid Plexus Tumors Reveals Novel Clinically Relevant Subgroups

43. Supplementary Materials and Methods from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

44. Supplementary Fig 6 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

45. Data from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

46. Supplementary Figures 1 - 2 from Phase I Study of Vismodegib in Children with Recurrent or Refractory Medulloblastoma: A Pediatric Brain Tumor Consortium Study

47. Supplementary Table 2 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

48. Supplementary Fig 4 from Myc and Loss of p53 Cooperate to Drive Formation of Choroid Plexus Carcinoma

49. Supplementary Figure 1 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

50. Supplementary Figure 2 from Copy Number Gain of 1q25 Predicts Poor Progression-Free Survival for Pediatric Intracranial Ependymomas and Enables Patient Risk Stratification: A Prospective European Clinical Trial Cohort Analysis on Behalf of the Children's Cancer Leukaemia Group (CCLG), Société Française d'Oncologie Pédiatrique (SFOP), and International Society for Pediatric Oncology (SIOP)

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