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229 results on '"McCormick, Frank"'

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1. Abstract A016: Expanded RAS proteoform landscape in malignant cell lines revealed by top-down mass spectrometry

2. Abstract A018: A top-down proteomic assay to evaluate KRAS4B-compound engagement

6. Abstract A028: An isogenic H/N/KRAS-less mouse embryonic fibroblast cell line panel derived from a size sorted diploid clonal parent

7. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

8. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

9. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

10. Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

11. Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

12. Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

13. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

14. Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

15. Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

16. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

17. Supplementary Data from Inhibition of MET Signaling with Ficlatuzumab in Combination with Chemotherapy in Refractory AML: Clinical Outcomes and High-Dimensional Analysis

18. Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

19. Supplementary Table S5 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

20. Supplementary Table S4 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

26. Supplementary Methods, Table Legends, Figures 1 - 7 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

30. Supplementary Methods, Table Legends, Figures 1 - 7 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

32. Data from Development of siRNA Payloads to Target KRAS-Mutant Cancer

38. Data from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

40. Supplementary Table S5 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

47. Supplementary Table S3 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

49. Supplementary Table S2 from Linking Tumor Mutations to Drug Responses via a Quantitative Chemical–Genetic Interaction Map

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