132 results on '"Claudio Isella"'
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2. Multi-label transcriptional classification of colorectal cancer reflects tumor cell population heterogeneity
3. Supplementary Table 3 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
4. Data from The Unfolded Protein Response: A Novel Therapeutic Target for Poor Prognostic BRAF Mutant Colorectal Cancer
5. Supplementary Figure 1 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
6. Supplementary Tables S1-S4 from The Unfolded Protein Response: A Novel Therapeutic Target for Poor Prognostic BRAF Mutant Colorectal Cancer
7. Supplementary Figure 6 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
8. Supplementary materials and methods from The Unfolded Protein Response: A Novel Therapeutic Target for Poor Prognostic BRAF Mutant Colorectal Cancer
9. Supplementary Table 2 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
10. Supplementary Figure 5 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
11. Supplementary Table 1 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
12. Supplementary Figure 2 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
13. Supplementary Figure 4 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
14. Data from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
15. Supplementary Figure 3 from A Molecularly Annotated Platform of Patient-Derived Xenografts ('Xenopatients') Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
16. Data from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
17. Supplementary Tables from High USP6NL Levels in Breast Cancer Sustain Chronic AKT Phosphorylation and GLUT1 Stability Fueling Aerobic Glycolysis
18. Supplementary Figure 6 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
19. Figure S5 from High USP6NL Levels in Breast Cancer Sustain Chronic AKT Phosphorylation and GLUT1 Stability Fueling Aerobic Glycolysis
20. Supplementary Materials and Methods from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
21. Supplementary Data from Patient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal Cancer
22. Supplementary Experimental Procedures from A Molecularly Annotated Model of Patient-Derived Colon Cancer Stem–Like Cells to Assess Genetic and Nongenetic Mechanisms of Resistance to Anti-EGFR Therapy
23. Supplementary Figure S3 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits
24. Supplementary Table S1 from Patient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal Cancer
25. Supplementary Figure 3 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
26. Supplementary Table S1 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
27. Supplementary Table S3 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
28. Figure S6 from High USP6NL Levels in Breast Cancer Sustain Chronic AKT Phosphorylation and GLUT1 Stability Fueling Aerobic Glycolysis
29. Supplementary Table S4 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits
30. Supplementary Table S3 from A Subset of Colorectal Cancers with Cross-Sensitivity to Olaparib and Oxaliplatin
31. Supplementary Table S3 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits
32. Figure S1 from High USP6NL Levels in Breast Cancer Sustain Chronic AKT Phosphorylation and GLUT1 Stability Fueling Aerobic Glycolysis
33. Supplementary Legends and Figures from A Subset of Colorectal Cancers with Cross-Sensitivity to Olaparib and Oxaliplatin
34. Supplementary Figure S1 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
35. Figure S2 from High USP6NL Levels in Breast Cancer Sustain Chronic AKT Phosphorylation and GLUT1 Stability Fueling Aerobic Glycolysis
36. Supplementary Table S2 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
37. Supplementary Table S3 from Patient-Derived Xenografts and Matched Cell Lines Identify Pharmacogenomic Vulnerabilities in Colorectal Cancer
38. Supplementary Tables S1-S5 from A Molecularly Annotated Model of Patient-Derived Colon Cancer Stem–Like Cells to Assess Genetic and Nongenetic Mechanisms of Resistance to Anti-EGFR Therapy
39. Data from Molecular Subtyping Combined with Biological Pathway Analyses to Study Regorafenib Response in Clinically Relevant Mouse Models of Colorectal Cancer
40. Supplementary Materials and Methods from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
41. Supplementary Table S2 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits
42. Supplementary Table S4 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
43. Figure S7 from High USP6NL Levels in Breast Cancer Sustain Chronic AKT Phosphorylation and GLUT1 Stability Fueling Aerobic Glycolysis
44. Supplementary Figure 4 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
45. Supplementary Table S6 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
46. Supplementary Figure S1 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits
47. Supplementary Figure 1 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
48. Supplementary Table S5 from Genetic and Expression Analysis of MET, MACC1, and HGF in Metastatic Colorectal Cancer: Response to Met Inhibition in Patient Xenografts and Pathologic Correlations
49. Supplementary Figure 7 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
50. Supplementary Table S1 from A Comprehensive PDX Gastric Cancer Collection Captures Cancer Cell–Intrinsic Transcriptional MSI Traits
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