Search

Your search keyword '"Zabriskie, Matthew S."' showing total 167 results

Search Constraints

Start Over You searched for: Author "Zabriskie, Matthew S." Remove constraint Author: "Zabriskie, Matthew S."
167 results on '"Zabriskie, Matthew S."'

Search Results

2. MS4A3 promotes differentiation in chronic myeloid leukemia by enhancing common β-chain cytokine receptor endocytosis

4. Supplementary Figures from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

5. Supplementary Table 1 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

6. Supplementary Table 8 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

7. Supplementary Table 5 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

8. Supplementary Table 3 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

9. Supplementary Table 7 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

10. Data from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

11. Supplementary Table 6 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

12. Supplementary Table 4 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

13. Supplementary Table 2 from SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

14. Supplementary Figure S1 from A Novel Crizotinib-Resistant Solvent-Front Mutation Responsive to Cabozantinib Therapy in a Patient with ROS1-Rearranged Lung Cancer

15. Supplementary Figure Legends and Tables from A Novel Crizotinib-Resistant Solvent-Front Mutation Responsive to Cabozantinib Therapy in a Patient with ROS1-Rearranged Lung Cancer

16. Data from Threshold Levels of ABL Tyrosine Kinase Inhibitors Retained in Chronic Myeloid Leukemia Cells Determine Their Commitment to Apoptosis

17. Supplementary Methods from Threshold Levels of ABL Tyrosine Kinase Inhibitors Retained in Chronic Myeloid Leukemia Cells Determine Their Commitment to Apoptosis

18. Supplementary Figures 1 - 6 from Threshold Levels of ABL Tyrosine Kinase Inhibitors Retained in Chronic Myeloid Leukemia Cells Determine Their Commitment to Apoptosis

19. Supplementary Figure Legend from Threshold Levels of ABL Tyrosine Kinase Inhibitors Retained in Chronic Myeloid Leukemia Cells Determine Their Commitment to Apoptosis

20. Supplementary Tables 1 - 2 from Threshold Levels of ABL Tyrosine Kinase Inhibitors Retained in Chronic Myeloid Leukemia Cells Determine Their Commitment to Apoptosis

22. shRNA library screening identifies nucleocytoplasmic transport as a mediator of BCR-ABL1 kinase-independent resistance

24. BCR-ABL1 Compound Mutations Combining Key Kinase Domain Positions Confer Clinical Resistance to Ponatinib in Ph Chromosome-Positive Leukemia

25. BCR-ABL1 compound mutations in tyrosine kinase inhibitor–resistant CML: frequency and clonal relationships

26. Spatially resolved transcriptomics for evaluation of intracranial vessels in a rabbit model: Proof of concept.

31. MS4A3 Promotes Differentiation in Chronic Myeloid Leukemia By Enhancing Common β Chain Cytokine Receptor Endocytosis

32. Abstract LB109: A critical role for SIRT5 in acute myeloid leukemia metabolism

33. SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

34. SIRT5 Is a Druggable Metabolic Vulnerability in Acute Myeloid Leukemia

37. sj-pdf-1-neu-10.1177_1971400920980153 - Supplemental material for Rabbit models of intracranial atherosclerotic disease for pathological validation of vessel wall MRI

38. Combining the Allosteric ABL1 Inhibitor Asciminib (ABL001) with Ponatinib Suppresses Emergence of and Restores Efficacy Against Highly Resistant BCR-ABL1 Compound Mutants

39. Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants

40. Rabbit models of intracranial atherosclerotic disease for pathological validation of vessel wall MRI.

41. A novel AGGF1-PDGFRb fusion in pediatric T-cell acute lymphoblastic leukemia

42. Characterization of the Genomic Landscape of BCR-ABL1 Kinase-Independent Mechanisms of Resistance to ABL1 Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia

43. A Novel Crizotinib-Resistant Solvent-Front Mutation Responsive to Cabozantinib Therapy in a Patient with ROS1-Rearranged Lung Cancer

46. Next Generation Sequencing to Delineate the Mutational Landscape of Chronic Myelomonocytic Leukemia (CMML): Novel Disease Genes and Correlations with Survival

47. BP5-087, a Novel STAT3 Inhibitor, Combines With BCR-ABL1 Inhibition To Overcome Kinase-Independent Resistance In Chronic Myeloid Leukemia

48. An Unbiased shRNA Library Screen Identifies Nucleocytoplasmic Transport As a Potential Target For Treatment Of Chronic Myeloid Leukemia

49. Threshold Levels of ABL Tyrosine Kinase Inhibitors Retained in Chronic Myeloid Leukemia Cells Determine Their Commitment to Apoptosis

50. STAT3 Inhibition Synergizes with BCR-ABL1 Inhibition to Overcome Kinase-Independent TKI Resistance in Chronic Myeloid Leukemia (CML)

Catalog

Books, media, physical & digital resources