80 results on '"Mancias, Joseph D"'
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2. Arm B count matrices 4 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
3. Data from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
4. Arm A count matrices 3 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
5. Table S1 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
6. Supplementary Data 1 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
7. Arm A count matrices 3 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
8. TCR raw data 2 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
9. TCR raw data 2 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
10. Arm B count matrices 4 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
11. Data from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
12. Table S1 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
13. Abstract C053: Autophagy regulates MAT2A in response to hypoxia in pancreatic cancer cells
14. Abstract B052: Defining the lysosome proteome during tumor evolution
15. PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer
16. Supplementary Table from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
17. Supplementary Figure from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
18. Data from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
19. Supplementary Data from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
20. Supplementary Table from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
21. Supplementary Data from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer
22. Data from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
23. Supplementary Figure from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
24. Data from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer
25. Supplementary Table from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
26. Supplementary Figure from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer
27. Supplementary Figure from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer
28. Supplementary Table from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
29. Supplementary Table from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
30. Supplementary Data from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
31. Data from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer
32. Supplementary Table from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins
33. Supplementary Data from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer
34. Data from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
35. Supplementary Figure S3 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
36. Data from An In Vivo CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML
37. Supplementary Tables from An In Vivo CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML
38. Supplementary Figure S4 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
39. Supplementary Data from An In Vivo CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML
40. Data from Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer
41. Supplementary Figure S2 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
42. Supplementary Data from An In Vivo CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML
43. Supplemental Figure S1 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
44. Supplementary Table S1 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
45. Data from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
46. Data from An In Vivo CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML
47. Supplementary Data from Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer
48. Supplementary Table S1 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
49. Supplementary Data from Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer
50. Supplementary Figure S2 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer
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