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1. Efficient and Accurate Quantized Image Super-Resolution on Mobile NPUs, Mobile AI & AIM 2022 Challenge: Report

2. Putting the STING back into BH3-mimetic drugs for TP53-mutant blood cancers

3. Olutasidenib in post-venetoclax patients with mutant isocitrate dehydrogenase 1 (m IDH1 ) acute myeloid leukemia (AML)

4. Targeting Molecular Measurable Residual Disease and Low-Blast Relapse in AML With Venetoclax and Low-Dose Cytarabine: A Prospective Phase II Study (VALDAC)

5. Single-cell Rapid Capture Hybridization sequencing (scRaCH-seq) to reliably detect isoform usage and coding mutations in targeted genes at a single-cell level

7. Sorafenib plus intensive chemotherapy in newly diagnosed FLT3-ITD AML: a randomized, placebo-controlled study by the ALLG

8. Phase Ib study of sabatolimab (MBG453), a novel immunotherapy targeting TIM‐3 antibody, in combination with decitabine or azacitidine in high‐ or very high‐risk myelodysplastic syndromes

9. Survival outcomes in patients with acute myeloid leukaemia who received subsequent therapy for relapse in QUAZAR AML‐001

10. Cusatuzumab plus azacitidine in newly diagnosed acute myeloid leukaemia ineligible for intensive chemotherapy (CULMINATE): part one of a randomised, phase 2, dose optimisation study

12. Somatic mutational landscape of hereditary hematopoietic malignancies caused by germline variants in RUNX1, GATA2, and DDX41

14. Measurable residual disease monitoring in patients with acute myeloid leukemia treated with lower‐intensity therapy: Roadmap from an ELN‐DAVID expert panel

18. POSTER: AML-370 Phase IB OMNIVERSE Trial: Safety and Tolerability of Oral Azacitidine (Oral-AZA) in Combination With Venetoclax (VEN) for Treatment of Acute Myeloid Leukemia (AML)

19. AML-370 Phase IB OMNIVERSE Trial: Safety and Tolerability of Oral Azacitidine (Oral-AZA) in Combination With Venetoclax (VEN) for Treatment of Acute Myeloid Leukemia (AML)

21. Molecular MRD is strongly prognostic in patients with NPM1-mutated AML receiving venetoclax-based non-intensive therapy

22. P459: DISEASE MONITORING OF NPM1-MUTANT (MUT) ACUTE MYELOID LEUKEMIA (AML) USING MEASURABLE RESIDUAL DISEASE (MRD) ASSESSMENTS DURING ORAL AZACITIDINE (ORAL-AZA) TREATMENT (TX): A QUAZAR AML-001 SUBANALYSIS

23. P365: SEQUENTIAL BLINATUMOMAB WITH REDUCED INTENSITY CHEMOTHERAPY FOR OLDER ADULTS WITH NEWLY DIAGNOSED PH- B-PRECURSOR ACUTE LYMPHOBLASTIC LEUKEMIA – FINAL RESULTS OF THE ALLG ALL08 STUDY

24. P567: PHASE 1B OMNIVERSE TRIAL: SAFETY AND TOLERABILITY OF ORAL AZACITIDINE IN COMBINATION WITH VENETOCLAX FOR TREATMENT OF ACUTE MYELOID LEUKEMIA

26. Updates in classification, risk stratification and response assessment in myelodysplastic syndromes/neoplasms (MDS): A state-of-the-art report on behalf of the International Consortium of MDS (icMDS)

27. P418: DELE1 LOSS AND DYSFUNCTIONAL INTEGRATED STRESS SIGNALING IN TP53 MUTATED AML IS A NOVEL PATHWAY FOR VENETOCLAX RESISTANCE

28. P411: LONGITUDINAL CHARACTERIZATION OF MOLECULAR VARIANTS AT REMISSION AND RELAPSE: SUBANALYSIS OF THE QUAZAR AML-001 TRIAL

29. Data from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

30. Supplementary Information v.2 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

31. Supplementary Figures S1-S22 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

32. Supplementary Table S15 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

33. Supplementary Figures S1-S22 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

34. Supplementary Figures S1-S22 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

35. Olutasidenib (FT-2102) induces durable complete remissions in patients with relapsed or refractory IDH1-mutated AML

36. Supplementary Figures S1-S22 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

37. Supplementary Figures S1-S22 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

38. Supplementary Table S11 from C/EBPα Confers Dependence to Fatty Acid Anabolic Pathways and Vulnerability to Lipid Oxidative Stress–Induced Ferroptosis in FLT3-Mutant Leukemia

40. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

41. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

42. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

43. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

44. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

45. Data from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

46. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

47. Abstract 2530: DELE1 loss and dysfunctional integrated stress signaling in TP53 mutated AML is a novel pathway for venetoclax resistance

48. Supplementary Figure from Pharmacologic Reduction of Mitochondrial Iron Triggers a Noncanonical BAX/BAK-Dependent Cell Death

49. Supplementary Table from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

50. Supplementary Figure from Epigenetic Activation of Plasmacytoid DCs Drives IFNAR-Dependent Therapeutic Differentiation of AML

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