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5. Fusion partner–specific mutation profiles and KRAS mutations as adverse prognostic factors in MLL-rearranged AML

6. Transcriptome analysis offers a comprehensive illustration of the genetic background of pediatric acute myeloid leukemia

7. P527: DISTINCTIVE CLONAL EVOLUTION PATTERN AND PROGNOSTIC SIGNIFICANCE OF THE CLONALITY OF KRAS MUTATIONS IN KMT2A-REARRANGED ACUTE MYELOID LEUKEMIA

9. RUNX1–Survivin Axis Is a Novel Therapeutic Target for Malignant Rhabdoid Tumors

10. Genetic regulation of the RUNX transcription factor family has antitumor effects

11. RUNX1 transactivates BCR‐ABL1 expression in Philadelphia chromosome positive acute lymphoblastic leukemia

12. Clonal Evolution Pattern and Prognostic Significance of Clonal Architecture in KMT2A-Rearranged Acute Myeloid Leukemia

14. RUNX inhibitor suppresses graft‐versus‐host disease through targeting RUNX‐NFATC2 axis

15. Clinical significance of RAS pathway alterations in pediatric acute myeloid leukemia

16. RUNX-NFAT Axis As a Novel Therapeutic Target for AML and T Cell Immunity

17. KRAS mutations Frequently Coexist with High-Risk MLL Fusions and Are Independent Adverse Prognostic Factors in MLL-Rearranged Acute Myeloid Leukemia

19. RUNX1 transactivates BCR‐ABL1 expression in Philadelphia chromosome positive acute lymphoblastic leukemia.

21. The Detection of Minor Clones with Somatic KIT D816V Mutations Using Droplet Digital PCR in Pediatric De Novo AML: AML-05 Trial from the Japanese Pediatric Leukemia/Lymphoma Study Group

22. Clinical Features of Pediatric Acute Myeloid Leukemia with TP53 and CDKN2A/2B copy Number Alterations

23. Coexistence and Prognostic Significance of EVI1 Expression and Driver Mutations in KMT2A-Rearranged Acute Myeloid Leukemia

24. Recurrent Gene Mutations in Pediatric Patients with AML By Targeted Sequencing ―the Jccg Study, JPLSG AML-05―

26. EVI1 triggers metabolic reprogramming associated with leukemogenesis and increases sensitivity to L-asparaginase

27. Comprehensive Analysis of 343 Genes Using Targeted Sequencing Panel By Next-Generation Sequencer in 77 Pediatric AML Patients with Normal and Complex Karyotypes: Jccg Study, JPLSG AML-05

28. Recurrent Genomic Aberrations of D-Type Cyclins Are Therapeutic Targets of CDK4/6 Inhibitors in t(8;21) and MLL-Rearranged Acute Myeloid Leukemia

30. Recurrent CCND3 mutations in MLL-rearranged acute myeloid leukemia

32. Autonomous feedback loop of RUNX1-p53-CBFB in acute myeloid leukemia cells

35. Fusion partner–specific mutation profiles and KRASmutations as adverse prognostic factors in MLL-rearranged AML

36. Label-Free Cell Detection of Acute Leukemia Using High-Content Morphological Profiling in Flow

37. Suppression of Super-Enhancer-Driven TAL1Expression By KLF4 in T-Cell Acute Lymphoblastic Leukemia

38. Prognostic Significance of CXCR4 Overexpression in Pediatric Acute Myeloid Leukemia with Low-Risk: A Report from the Japanese Pediatric Leukemia/Lymphoma Study Group

40. Enhancement of neutrophil autophagy by an IVIG preparation against multidrug-resistant bacteria as well as drug-sensitive strains

41. Double CEBPA Mutations Are Not Associated With Favorable Clinical Outcome In Pediatric AML: A Report From The Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG)

42. KRASmutations Frequently Coexist with High-Risk MLLFusions and Are Independent Adverse Prognostic Factors in MLL-Rearranged Acute Myeloid Leukemia

43. Clinical Features of Pediatric Acute Myeloid Leukemia with TP53and CDKN2A/2Bcopy Number Alterations

45. Prognostic Significance of CXCR4Overexpression in Pediatric Acute Myeloid Leukemia with Low-Risk: A Report from the Japanese Pediatric Leukemia/Lymphoma Study Group

46. Double CEBPAMutations Are Not Associated With Favorable Clinical Outcome In Pediatric AML: A Report From The Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG)

47. Clinical significance of RAS pathway alterations in pediatric acute myeloid leukemia.

48. EVI1 triggers metabolic reprogramming associated with leukemogenesis and increases sensitivity to L-asparaginase.

50. EVI1 overexpression is a poor prognostic factor in pediatric patients with mixed lineage leukemia-AF9 rearranged acute myeloid leukemia.

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