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1. RNA binding protein SYNCRIP maintains proteostasis and self-renewal of hematopoietic stem and progenitor cells

4. TP53 mutations and RNA-binding protein MUSASHI-2 drive resistance to PRMT5-targeted therapy in B-cell lymphoma

6. Transcriptional control of CBX5 by the RNA-binding proteins RBMX and RBMXL1 maintains chromatin state in myeloid leukemia

10. SON is an essential m6A target for hematopoietic stem cell fate

11. Metabolic adaptation of acute lymphoblastic leukemia to the central nervous system microenvironment depends on stearoyl-CoA desaturase

13. ChromaFold predicts the 3D contact map from single-cell chromatin accessibility

14. Supplementary Tables 1-6 from Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia

15. Data from Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia

16. Supplementary Figures 1-8 from Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia

19. The N6-methyladenosine (m6A)-forming enzyme METTL3 controls myeloid differentiation of normal hematopoietic and leukemia cells

20. Patient-Derived iPSCs Faithfully Represent the Genetic Diversity and Cellular Architecture of Human Acute Myeloid Leukemia

21. Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

22. Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

23. Supplementary Figures from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

24. Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

25. Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis

26. Supplementary Materials and Methods from Therapeutic Efficacy of an Fc-Enhanced TCR-like Antibody to the Intracellular WT1 Oncoprotein

27. Data from Epigenetically Aberrant Stroma in MDS Propagates Disease via Wnt/β-Catenin Activation

28. Supplementary Figure 3 from Therapeutic Efficacy of an Fc-Enhanced TCR-like Antibody to the Intracellular WT1 Oncoprotein

29. Supplementary Figure 1 from Therapeutic Efficacy of an Fc-Enhanced TCR-like Antibody to the Intracellular WT1 Oncoprotein

30. Supplementary Figure 4 from Therapeutic Efficacy of an Fc-Enhanced TCR-like Antibody to the Intracellular WT1 Oncoprotein

31. Supplementary Table 1 from Therapeutic Efficacy of an Fc-Enhanced TCR-like Antibody to the Intracellular WT1 Oncoprotein

32. Supplementary Figure 2 from Therapeutic Efficacy of an Fc-Enhanced TCR-like Antibody to the Intracellular WT1 Oncoprotein

33. Supp tables 1-5 from Epigenetically Aberrant Stroma in MDS Propagates Disease via Wnt/β-Catenin Activation

34. Supp Methods from Epigenetically Aberrant Stroma in MDS Propagates Disease via Wnt/β-Catenin Activation

35. Supp Figs 1-5 from Epigenetically Aberrant Stroma in MDS Propagates Disease via Wnt/β-Catenin Activation

36. Small-molecule targeting of MUSASHI RNA-binding activity in acute myeloid leukemia

37. BTG1 mutation yields supercompetitive B cells primed for malignant transformation

38. Fructose Treatment Targets Myeloid Leukemogenesis in IDH2 Mutants By Exhausting Alpha-Ketoglutarate Pools

40. Dual IKZF2 and CK1α Degrader Targets Acute Myeloid Leukemia Cells

41. Abstract A24: BTG1 mutations confer a fitness advantage and promote aggressive B cell lymphoma development by lowering the threshold for MYC induction

42. In Vivo RNAi Screening Identifies a Leukemia-Specific Dependence on Integrin Beta 3 Signaling

43. Musashi2 sustains the mixed-lineage leukemia-driven stem cell regulatory program

47. BTG1 Mutation Promotes Aggressive Lymphoma Development By Lowering the Threshold to MYC Activation and Generating "Super-Competitor" B Cells

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