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1. Multi-gene measurable residual disease assessed by digital polymerase chain reaction has clinical and biological utility in acute myeloid leukemia patients receiving venetoclax/azacitidine

2. Therapy-Resistant Acute Myeloid Leukemia Stem Cells Are Resensitized to Venetoclax + Azacitidine by Targeting Fatty Acid Desaturases 1 and 2

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3. Real-world experience of venetoclax with azacitidine for untreated patients with acute myeloid leukemia

4. Enriching for human acute myeloid leukemia stem cells using reactive oxygen species-based cell sorting

5. 309 MYC Inhibition Overcomes IMiD Resistance in Heterogeneous Multiple Myeloma Populations

6. Characterization and targeting of malignant stem cells in patients with advanced myelodysplastic syndromes

7. Pro-inflammatory cytokine blockade attenuates myeloid expansion in a murine model of rheumatoid arthritis

8. The Hematopoietic Oxidase NOX2 Regulates Self-Renewal of Leukemic Stem Cells

9. Inhibition of redox/Fyn/c‐Cbl pathway function by Cdc42 controls tumour initiation capacity and tamoxifen sensitivity in basal‐like breast cancer cells

10. Data from The Hepatic Microenvironment Uniquely Protects Leukemia Cells through Induction of Growth and Survival Pathways Mediated by LIPG

11. Data from Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia

12. Supplementary Figures S1-S5 from Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia

13. Supplementary Data from The Hepatic Microenvironment Uniquely Protects Leukemia Cells through Induction of Growth and Survival Pathways Mediated by LIPG

14. Supplementary Tables S1-S6 from Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia

15. Supplemental Methods from Tyrosine Kinase Inhibition in Leukemia Induces an Altered Metabolic State Sensitive to Mitochondrial Perturbations

17. Supplemental Tables 1-4 from Tyrosine Kinase Inhibition in Leukemia Induces an Altered Metabolic State Sensitive to Mitochondrial Perturbations

18. Data from Exploiting Protein Translation Dependence in Multiple Myeloma with Omacetaxine-Based Therapy

19. Supplemental Figures 1-8 from Tyrosine Kinase Inhibition in Leukemia Induces an Altered Metabolic State Sensitive to Mitochondrial Perturbations

20. Data from Tyrosine Kinase Inhibition in Leukemia Induces an Altered Metabolic State Sensitive to Mitochondrial Perturbations

21. Venetoclax and azacitidine compared with induction chemotherapy for newly diagnosed patients with acute myeloid leukemia

22. A novel type of monocytic leukemia stem cell revealed by the clinical use of venetoclax-based therapy

23. MuVEH and mitoMuVEH improve discovery of genetic variation from single cells

24. The Intriguing Clinical Success of BCL-2 Inhibition in Acute Myeloid Leukemia

25. MDS-associated SF3B1 mutations enhance proinflammatory gene expression in patient blast cells

26. Fatty acid metabolism underlies venetoclax resistance in acute myeloid leukemia stem cells

27. Monocytic Subclones Confer Resistance to Venetoclax-Based Therapy in Patients with Acute Myeloid Leukemia

29. Higher-Dose Venetoclax with Measurable Residual Disease-Guided Azacitidine Discontinuation in Newly Diagnosed Patients with Acute Myeloid Leukemia: Phase 2 Hiddav Study

30. Intracellular Calcium Localization Mediates the Activity of Venetoclax in Targeting Acute Myeloid Leukemia Stem Cells

32. Sequential azacitidine and lenalidomide for patients with relapsed and refractory acute myeloid leukemia: Clinical results and predictive modeling using computational analysis

33. Low ferroportin expression in AML is correlated with good risk cytogenetics, improved outcomes and increased sensitivity to chemotherapy

34. The STAT3-MYC axis promotes survival of leukemia stem cells by regulating SLC1A5 and oxidative phosphorylation

35. PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress

36. Enriching for human acute myeloid leukemia stem cells using reactive oxygen species-based cell sorting

37. Exploiting Protein Translation Dependence in Multiple Myeloma with Omacetaxine-based Therapy

38. ETV6 germline mutations cause HDAC3/NCOR2 mislocalization and upregulation of interferon response genes

39. Nicotinamide Metabolism Mediates Resistance to Venetoclax in Relapsed Acute Myeloid Leukemia Stem Cells

40. PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress

41. Abstract 3956: MYC inhibition overcomes IMiD resistance in heterogeneous multiple myeloma populations

42. Prolonged Omacetaxine Treatment Alters Fitness and Proteostasis in Multiple Myeloma

43. Unique Metabolic Vulnerabilities of Myelodysplastic Syndrome Stem Cells

44. Targeting MDS Stem Cells with Omacetaxine and Azacitidine for Newly Diagnosed High Grade Patients: Phase 1 Trial Results and Preliminary Mechanistic Studies

45. Lysosomal Acid Lipase a (LIPA) Modulates Leukemia Stem Cell (LSC) Response to Venetoclax/TKI Combination Therapy in Blast Phase Chronic Myeloid Leukemia

46. The Hepatic Microenvironment Uniquely Protects Leukemia Cells through Induction of Growth and Survival Pathways Mediated by LIPG

47. Measurement of ex vivo resistance to proteasome inhibitors, IMiDs, and daratumumab during multiple myeloma progression

48. Pro-inflammatory cytokine blockade attenuates myeloid expansion in a murine model of rheumatoid arthritis

49. Rational Design of a Parthenolide-based Drug Regimen That Selectively Eradicates Acute Myelogenous Leukemia Stem Cells

50. Evolution of acute myelogenous leukemia stem cell properties after treatment and progression