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2. Targeting Acute Myeloid Leukemia Stem Cells Through Perturbation of Mitochondrial Calcium

4. AMPK/FIS1-Mediated Mitophagy Is Required for Self-Renewal of Human AML Stem Cells

6. Targeting Acute Myeloid Leukemia Stem Cells Through Perturbation of Mitochondrial Calcium

7. Supplementary Table 6 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

8. Supplementary Table 2 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

9. Supplementary Table 8 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

10. Supplementary Tables 3-5 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

11. Supplementary Table 7 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

12. Supplementary Table 1 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

13. Supplementary Table 9 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

14. Supplementary Figures S1-S7 from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

15. Data from A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

16. Venetoclax with azacitidine disrupts energy metabolism and targets leukemia stem cells in patients with acute myeloid leukemia

17. A Novel Type of Monocytic Leukemia Stem Cell Revealed by the Clinical Use of Venetoclax-Based Therapy

18. In silico predicted compound targeting the IQGAP1-GRD domain selectively inhibits growth of human acute myeloid leukemia

19. Higher-dose venetoclax with measurable residual disease-guided azacitidine discontinuation in newly diagnosed acute myeloid leukemia

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

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

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

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

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

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

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

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

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

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

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

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

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

35. Developmental Plasticity of Acute Myeloid Leukemia Mediates Resistance to Venetoclax-Based Therapy

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

38. Subversion of Systemic Glucose Metabolism as a Mechanism to Support the Growth of Leukemia Cells

39. Targeted therapy for a subset of acute myeloid leukemias that lack expression of aldehyde dehydrogenase 1A1

43. Rational design of a parthenolide-based drug regimen that selectively eradicates acute myelogenous leukemia stem cells.

44. Leukemic Stem Cells Evade Chemotherapy by Metabolic Adaptation to an Adipose Tissue Niche

50. Rotational Rheometry of Liquid Metal Systems: A Study with Al-Si Hypoeutectic Alloys

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