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2. Phase 1 study of JNJ-64619178, a protein arginine methyltransferase 5 inhibitor, in patients with lower-risk myelodysplastic syndromes

3. Supplementary Figure 1 from Phase 1 Study of JNJ-64619178, a Protein Arginine Methyltransferase 5 Inhibitor, in Advanced Solid Tumors

4. Supplementary Tables 1-3 from Phase 1 Study of JNJ-64619178, a Protein Arginine Methyltransferase 5 Inhibitor, in Advanced Solid Tumors

5. Data from Phase 1 Study of JNJ-64619178, a Protein Arginine Methyltransferase 5 Inhibitor, in Advanced Solid Tumors

6. Phase 1 Study of JNJ-64619178, a Protein Arginine Methyltransferase 5 Inhibitor, in Advanced Solid Tumors

7. Acute megakaryoblastic leukaemia shows high frequency of chromosome 1q aberrations and dismal outcome

8. Data from PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2V617F-Mutant MPN

9. Supplementary Data from PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2V617F-Mutant MPN

10. Supplementary Figures from Evolution of Cytogenetically Normal Acute Myeloid Leukemia During Therapy and Relapse: An Exome Sequencing Study of 50 Patients

11. Table S4 from Evolution of Cytogenetically Normal Acute Myeloid Leukemia During Therapy and Relapse: An Exome Sequencing Study of 50 Patients

12. Phase 1 study of JNJ-64619178, a protein arginine methyltransferase 5 inhibitor, in patients with lower-risk myelodysplastic syndromes

13. DNMT3A mutations promote anthracycline resistance in acute myeloid leukemia via impaired nucleosome remodeling

14. Molecular profiling of patients with cytogenetically normal acute myeloid leukemia and hyperleukocytosis

15. Phase 1 Study of JNJ-64619178, a Protein Arginine Methyltransferase 5 Inhibitor, in Patients with Lower-Risk Myelodysplastic Syndromes

16. Discovery and Pharmacological Characterization of JNJ-64619178, a Novel Small-Molecule Inhibitor of PRMT5 with Potent Antitumor Activity

18. PRMT5 inhibition modulates E2F1 methylation and gene regulatory networks leading to therapeutic efficacy in JAK2V617F mutant MPN

19. PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2V617F-Mutant MPN

21. PRMT5 Inhibition Modulates E2F1 Methylation and Gene Regulatory Networks Leading to Therapeutic Efficacy in JAK2VF Mutant MPN

22. PHF6 and DNMT3A mutations are enriched in distinct subgroups of mixed phenotype acute leukemia with T-lineage differentiation

23. PHF6 Mutations Are Mutually Exclusive to TP53 Mutations, and Define a Distinct Subgroup of Secondary Acute Myeloid Leukemia Associated with a Primitive Stem/Progenitor Immunophenotype, Absent Complex Karyotype and Relatively Better Outcomes

24. Targeting the CALR interactome in myeloproliferative neoplasms

25. Genetic heterogeneity of cytogenetically normal AML with mutations of CEBPA

26. Evolution of Cytogenetically Normal Acute Myeloid Leukemia During Therapy and Relapse: An Exome Sequencing Study of 50 Patients

27. Evolutionary Patterns of Cytogenetically Normal Acute Myeloid Leukemia Correlate with Time to Relapse

28. Mutations of Genes Linked to Epigenetic Regulation Are Frequently Gained in Relapsed Cytogenetically Normal Acute Myeloid Leukemia

29. PHF6and DNMT3Amutations are enriched in distinct subgroups of mixed phenotype acute leukemia with T-lineage differentiation

31. Genetic Evolution of Cytogenetically Normal Acute Myeloid Leukemia (CN-AML) during Therapy and Relapse: An Exome Sequencing Study of 47 Cases

32. The NPM1 Mutation Type Has No Impact on Survival in Cytogenetically Normal AML

33. Long-term follow-up of cytogenetically normal CEBPA-mutated AML

35. Combined Molecular and Clinical Prognostic Index for Relapse and Survival in Cytogenetically Normal Acute Myeloid Leukemia

37. Activating FLT3 Mutants Show Distinct Gain-of-Function Phenotypes In Vitro and a Characteristic Signaling Pathway Profile Associated with Prognosis in Acute Myeloid Leukemia

38. A Combined Molecular and Clinical Prognostic Index For Relapse and Survival In Cytogenetically Normal AML (PINA)

40. Long-term follow-up of cytogenetically normal CEBPA-mutated AML

41. Impressive thrombocytosis evolving in a patient with a BCR-ABL positive CML in major molecular response during dasatinib treatment unmasks an additional JAK2V617F

42. PHF6Mutations Are Mutually Exclusive to TP53Mutations, and Define a Distinct Subgroup of Secondary Acute Myeloid Leukemia Associated with a Primitive Stem/Progenitor Immunophenotype, Absent Complex Karyotype and Relatively Better Outcomes

43. PHF6Mutations Defines a Subgroup of Mixed Phenotype of Acute Leukemia with Aberrant T-Cell Differentiation

44. PRMT5 Inhibition Modulates E2F1 Methylation and Gene-Regulatory Networks Leading to Therapeutic Efficacy in JAK2 V617F -Mutant MPN.

45. Epigenetic regulators and their impact on therapy in acute myeloid leukemia.

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