251 results on '"Lamba, Simona"'
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2. Non-canonical antigens are the largest fraction of peptides presented by MHC class I in mismatch repair deficient murine colorectal cancer
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
5. A modified fluctuation-test framework characterizes the population dynamics and mutation rate of colorectal cancer persister cells
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
31. Data from Novel Somatic and Germline Mutations in Cancer Candidate Genes in Glioblastoma, Melanoma, and Pancreatic Carcinoma
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
35. Supplementary Table 1 from Novel Somatic and Germline Mutations in Cancer Candidate Genes in Glioblastoma, Melanoma, and Pancreatic Carcinoma
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
39. Dual VEGFA/BRAF targeting boosts PD-1 blockade in melanoma through GM-CSF-mediated infiltration of M1 macrophages
40. RAF Suppression Synergizes with MEK Inhibition in KRAS Mutant Cancer Cells
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
45. Replacement of Normal with Mutant Alleles in the Genome of Normal Human Cells Unveils Mutation-Specific Drug Responses
46. The prognostic IDH1 R132 mutation is associated with reduced NADP+-dependent IDH activity in glioblastoma
47. Integrated molecular dissection of the epidermal growth factor receptor (EFGR) oncogenic pathway to predict response to EGFR-targeted monoclonal antibodies in metastatic 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
50. Targeted Knock-in of the Polymorphism rs61764370 Does Not Affect KRAS Expression but Reduces let-7 Levels
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