516 results on '"Stern, David F"'
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2. Identifying modules of cooperating cancer drivers
3. ErbB2 Is Required for Ductal Morphogenesis of the Mammary Gland
4. Neural and Mammary Gland Defects in ErbB4 Knockout Mice Genetically Rescued from Embryonic Lethality
5. p90RSK Blockade Inhibits Dual BRAF and MEK Inhibitor-Resistant Melanoma by Targeting Protein Synthesis
6. ErbB4 Signaling in the Mammary Gland Is Required for Lobuloalveolar Development and Stat5 Activation during Lactation
7. Supplementary Table 8 from Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening
8. Supplemental Figure 7 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
9. Supplementary Figure 1 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
10. Data from Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening
11. Supplemental Figure 1 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
12. Data from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
13. Supplementary Table S5 from Combinatorial Screening of Pancreatic Adenocarcinoma Reveals Sensitivity to Drug Combinations Including Bromodomain Inhibitor Plus Neddylation Inhibitor
14. Data from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
15. Supplementary Table 5 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
16. Data from NFBD1/MDC1 Regulates Cav1 and Cav2 Independently of DNA Damage and p53
17. Supplemental Figure 9 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
18. Supplementary Tables 1-3 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
19. Supplemental Figure 5 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
20. Supplementary Tables 1-7, 9 from Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening
21. Supplemental Figure 4 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
22. Supplementary Table 3 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
23. Supplementary Figure S1 from Combinatorial Screening of Pancreatic Adenocarcinoma Reveals Sensitivity to Drug Combinations Including Bromodomain Inhibitor Plus Neddylation Inhibitor
24. Supplementary Figure 1 from NFBD1/MDC1 Regulates Cav1 and Cav2 Independently of DNA Damage and p53
25. Supplemental Figure 2 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
26. Supplementary Figure 3 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
27. Supplementary Table 1 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
28. Supplementary Table 2 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
29. Supplemental Figure 6 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
30. Data from Combinatorial Screening of Pancreatic Adenocarcinoma Reveals Sensitivity to Drug Combinations Including Bromodomain Inhibitor Plus Neddylation Inhibitor
31. Supplementary Figure 1 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
32. Supplemental Figure 3 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
33. Supplementary Table 4 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
34. Supplementary figure and table legends from Combinatorial Screening of Pancreatic Adenocarcinoma Reveals Sensitivity to Drug Combinations Including Bromodomain Inhibitor Plus Neddylation Inhibitor
35. Supplementary Figure Legends, Table Legends from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
36. Supplementary Table 2 from NFBD1/MDC1 Regulates Cav1 and Cav2 Independently of DNA Damage and p53
37. Supplemental Table 1 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
38. Supplementary Legends for Figure 1 and Tables 1-2 from NFBD1/MDC1 Regulates Cav1 and Cav2 Independently of DNA Damage and p53
39. Supplementary Table 5 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
40. Supplemental Figure 8 from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
41. Data from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
42. Supplementary Figures 1-7 from Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening
43. Supplementary Table 1 from NFBD1/MDC1 Regulates Cav1 and Cav2 Independently of DNA Damage and p53
44. Supplemental Figure Legends from BRAF Inhibition Decreases Cellular Glucose Uptake in Melanoma in Association with Reduction in Cell Volume
45. Supplementary Table 6 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
46. Supplementary Figure 2 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
47. Supplementary Figure Legends 1-7, Table Legends 1-9 from Genotype-Selective Combination Therapies for Melanoma Identified by High-Throughput Drug Screening
48. Supplementary Table 4 from Convergent and Divergent Cellular Responses by ErbB4 Isoforms in Mammary Epithelial Cells
49. Supplementary Table Legends 1-6, Figure Legend 1 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
50. Supplementary Tables 2-13 from Acquired Resistance to HER2-Targeted Therapies Creates Vulnerability to ATP Synthase Inhibition
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