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1. DNA demethylation triggers cell free DNA release in colorectal cancer cells

3. Tolerance to colibactin correlates with homologous recombination proficiency and resistance to irinotecan in colorectal cancer cells

4. Genetic and pharmacological modulation of DNA mismatch repair heterogeneous tumors promotes immune surveillance

6. Adaptive mutability of colorectal cancers in response to targeted therapies

7. Preclinical efficacy of carfilzomib in BRAF‐mutant colorectal cancer models

8. Abstract B005: Tolerance to colibactin correlates with response to chemotherapeutic agents in colorectal cancer

9. Dual VEGFA/BRAF targeting boosts PD‐1 blockade in melanoma through GM‐CSF‐mediated infiltration of M1 macrophages

10. Abstract 5900: Tolerance to colibactin correlates with response to chemotherapeutic agents in colorectal cancer

11. Supplementary Figure 3 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

12. Supplementary Table 2 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

13. Supplementary Figure 2 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

14. Data from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

15. Supplementary Figure 4 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

16. Supplementary Table 3 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

17. Supplementary Table 1 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

18. Supplementary Figure 1 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

19. Supplementary Figure 2 from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

20. Supplementary Figure 3 from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

21. Data from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

22. Supplementary Figure from Targeting the DNA Damage Response Pathways and Replication Stress in Colorectal Cancer

23. Supplementary Material from BCAM and LAMA5 Mediate the Recognition between Tumor Cells and the Endothelium in the Metastatic Spreading of KRAS-Mutant Colorectal Cancer

24. Data from BCAM and LAMA5 Mediate the Recognition between Tumor Cells and the Endothelium in the Metastatic Spreading of KRAS-Mutant Colorectal Cancer

25. Supplementary Materials and Methods and Supplementary Figure Legends from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

26. Supplementary Figure 5 from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

27. Supplementary Table 1 from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

28. Supplementary Figure 4 from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

29. Supplementary Figure 1 from Nucleolin Targeting Impairs the Progression of Pancreatic Cancer and Promotes the Normalization of Tumor Vasculature

30. Supplementary Figure 4 from Mixed Lineage Kinase MLK4 Is Activated in Colorectal Cancers Where It Synergistically Cooperates with Activated RAS Signaling in Driving Tumorigenesis

32. Supplementary Table 1 from Mixed Lineage Kinase MLK4 Is Activated in Colorectal Cancers Where It Synergistically Cooperates with Activated RAS Signaling in Driving Tumorigenesis

33. Supplementary Figure 3 from Mixed Lineage Kinase MLK4 Is Activated in Colorectal Cancers Where It Synergistically Cooperates with Activated RAS Signaling in Driving Tumorigenesis

34. Supplementary Table 2 from Mixed Lineage Kinase MLK4 Is Activated in Colorectal Cancers Where It Synergistically Cooperates with Activated RAS Signaling in Driving Tumorigenesis

36. Supplementary Figure 1 from Mixed Lineage Kinase MLK4 Is Activated in Colorectal Cancers Where It Synergistically Cooperates with Activated RAS Signaling in Driving Tumorigenesis

37. Supplementary Figure 2 from Mixed Lineage Kinase MLK4 Is Activated in Colorectal Cancers Where It Synergistically Cooperates with Activated RAS Signaling in Driving Tumorigenesis

38. Supplementary Figure Legend from Mixed Lineage Kinase MLK4 Is Activated in Colorectal Cancers Where It Synergistically Cooperates with Activated RAS Signaling in Driving Tumorigenesis

41. Inactivation of DNA repair triggers neoantigen generation and impairs tumour growth

42. Clonal evolution and resistance to EGFR blockade in the blood of colorectal cancer patients

43. Targeting the DNA Damage Response Pathways and Replication Stress in Colorectal Cancer

44. Abstract 1593: Genetic and pharmacological modulation of DNA mismatch repair promotes immune surveillance in murine colorectal cancer

48. Association of KRAS p.G13D mutation with outcome in patients with chemotherapy-refractory metastatic colorectal cancer treated with cetuximab

49. CD4 T Cell–Dependent Rejection of Beta-2 Microglobulin Null Mismatch Repair–Deficient Tumors

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