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3. Supplementary Figure S1 from Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms

4. Supplementary Table S2 from Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms

5. Data from Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms

6. Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms

9. Supplementary Data1 from Development of Resistance to Type II JAK2 Inhibitors in MPN Depends on AXL Kinase and Is Targetable

10. Data from Development of Resistance to Type II JAK2 Inhibitors in MPN Depends on AXL Kinase and Is Targetable

11. Development of resistance to type II JAK2 inhibitors in MPN depends on AXL kinase and is targetable

12. Targeting compensatory MEK/ERK activation increases JAK inhibitor efficacy in myeloproliferative neoplasms

16. Escape from Type II JAK2 Inhibition in MPN Depends on AXL/MAPK Activation and Is Targetable

18. Interferon-γ resistance and immune evasion in glioma develop via Notch-regulated co-evolution of malignant and immune cells

21. Co-Occurring CSF3R W791* Germline and Somatic T618I Driver Mutations Induce Early CNL and Clonal Progression to Mixed Phenotype Acute Leukemia

23. Co-Occurring CSF3R W791* Germline and Somatic T618I Driver Mutations Induce Early CNL and Clonal Progression to Mixed Phenotype Acute Leukemia

29. Interferon-γ Resistance and Immune Evasion in Glioma Develop via Notch-Regulated Co-Evolution of Malignant and Immune Cells

34. Cooperative Epigenetic Remodeling by TET2 Loss and NRAS Mutation Drives Myeloid Transformation and MEK Inhibitor Sensitivity

36. In response to the comment by Hechler et al .: Amotosalen/UVA pathogen inactivation technology reduces platelet activatability, induces apoptosis and accelerates clearance.

42. Loss of Ezh2 synergizes with JAK2-V617F in initiating myeloproliferative neoplasms and promoting myelofibrosis

44. CHZ868, a Type II JAK2 Inhibitor, Reverses Type I JAK Inhibitor Persistence and Demonstrates Efficacy in Myeloproliferative Neoplasms

45. Type II Inhibition of JAK2 with NVP-CHZ868 Reverses Type I JAK Inhibitor Persistence and Demonstrates Increased Efficacy in MPN Models

49. Combined Targeting of JAK2 and Bcl-2/Bcl-xL to Cure Mutant JAK2-Driven Malignancies and Overcome Acquired Resistance to JAK2 Inhibitors

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