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2. Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS-MAPK Pathway Inhibition in Pancreatic Cancer.

3. Stereotactic MR-guided on-table adaptive radiation therapy (SMART) for borderline resectable and locally advanced pancreatic cancer: A multi-center, open-label phase 2 study

6. A Multi-Institutional Phase 2 Trial of Ablative 5-Fraction Stereotactic Magnetic Resonance-Guided On-Table Adaptive Radiation Therapy for Borderline Resectable and Locally Advanced Pancreatic Cancer

8. Autophagy promotes immune evasion of pancreatic cancer by degrading MHC-I

13. De novo pyrimidine biosynthesis inhibition synergizes with BCL-XLtargeting in pancreatic cancer

14. Recharacterization of RSL3 reveals that the selenoproteome is a druggable target in colorectal cancer

17. Supplementary Data 1 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer

18. 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

19. Data from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer

20. 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

21. Table S1 from PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer

22. 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

25. Stereotactic MR-guided on-table adaptive radiation therapy (SMART) for borderline resectable and locally advanced pancreatic cancer: a multi-center, open-label phase 2 study

26. Multiomic analysis on human cell model of wolfram syndrome reveals changes in mitochondrial morphology and function

27. Discovery of a selective inhibitor of doublecortin like kinase 1

30. PD-1 Blockade Induces Reactivation of Nonproductive T-Cell Responses Characterized by NF-κB Signaling in Patients with Pancreatic Cancer

32. Mutations in RABL3 alter KRAS prenylation and are associated with hereditary pancreatic cancer

37. Supplementary Table from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins

38. Supplementary Figure from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins

39. Data from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins

40. Supplementary Data from NCOA4-Mediated Ferritinophagy Is a Pancreatic Cancer Dependency via Maintenance of Iron Bioavailability for Iron–Sulfur Cluster Proteins

41. Supplementary Data from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer

42. Data from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer

43. Supplementary Figure from Coordinated Transcriptional and Catabolic Programs Support Iron-Dependent Adaptation to RAS–MAPK Pathway Inhibition in Pancreatic Cancer

44. Data from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer

45. Supplementary Figure S3 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 Tables from An In Vivo CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML

48. Supplementary Data from An In Vivo CRISPR Screening Platform for Prioritizing Therapeutic Targets in AML

49. Data from Selective Alanine Transporter Utilization Creates a Targetable Metabolic Niche in Pancreatic Cancer

50. Supplementary Table S1 from Selective Modulation of a Pan-Essential Protein as a Therapeutic Strategy in Cancer

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