1,232 results on '"Comoglio, Paolo"'
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2. EFECTIVIDAD, PRUEBAS Y NUEVAS TECNOLOGÍAS
3. Coexisting cancer stem cells with heterogeneous gene amplifications, transcriptional profiles, and malignancy are isolated from single glioblastomas
4. Correction: hOA-DN30: a highly effective humanized single-arm MET antibody inducing remission of ‘MET-addicted’ cancers
5. Efficacy of CAR-T immunotherapy in MET overexpressing tumors not eligible for anti-MET targeted therapy
6. hOA-DN30: a highly effective humanized single-arm MET antibody inducing remission of ‘MET-addicted’ cancers
7. The MET Oncogene: Thirty Years of Insights into Molecular Mechanisms Driving Malignancy
8. Factor XII protects neurons from apoptosis by epidermal and hepatocyte growth factor receptor‐dependent mechanisms
9. Correction to: Real-world histopathological approach to malignancy of undefined primary origin (MUO) to diagnose cancers of unknown primary (CUPs)
10. MET Oncogene Enhances Pro-Migratory Functions by Counteracting NMDAR2B Cleavage
11. Cancer of unknown primary stem-like cells model multi-organ metastasis and unveil liability to MEK inhibition
12. A receptor-antibody hybrid hampering MET-driven metastatic spread
13. Hepatocyte Growth Factor Receptor
14. Increased Lactate Secretion by Cancer Cells Sustains Non-cell-autonomous Adaptive Resistance to MET and EGFR Targeted Therapies
15. An Observatory for the MET Oncogene: A Guide for Targeted Therapies
16. An Observatory for the MET Oncogene; a Guide for Targeted Therapies
17. Reviving oncogenic addiction to MET bypassed by BRAF (G469A) mutation
18. Met inhibition revokes IFNγ-induction of PD-1 ligands in MET-amplified tumours
19. MET Oncogene Enhances Pro-Migratory Functions by Counteracting NMDAR2B Cleavage.
20. Uncoupling Signal Transducers from Oncogenic MET Mutants Abrogates Cell Transformation and Inhibits Invasive Growth
21. Known and novel roles of the MET oncogene in cancer: a coherent approach to targeted therapy
22. A Point Mutation in the MET Oncogene Abrogates Metastasis without Affecting Transformation
23. Ezrin Is an Effector of Hepatocyte Growth Factor-Mediated Migration and Morphogenesis in Epithelial Cells
24. Supplementary Figure S2 from Amplification of the MET Receptor Drives Resistance to Anti-EGFR Therapies in Colorectal Cancer
25. Supplementary Data 2 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation
26. 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
27. 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
28. Supplementary Figure S1 from S49076 Is a Novel Kinase Inhibitor of MET, AXL, and FGFR with Strong Preclinical Activity Alone and in Association with Bevacizumab
29. 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
30. Supplementary Figure Legends from S49076 Is a Novel Kinase Inhibitor of MET, AXL, and FGFR with Strong Preclinical Activity Alone and in Association with Bevacizumab
31. 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
32. Supplementary Table S1 from S49076 Is a Novel Kinase Inhibitor of MET, AXL, and FGFR with Strong Preclinical Activity Alone and in Association with Bevacizumab
33. 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
34. 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
35. Data from A Molecularly Annotated Platform of Patient-Derived Xenografts (“Xenopatients”) Identifies HER2 as an Effective Therapeutic Target in Cetuximab-Resistant Colorectal Cancer
36. 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
37. Supplementary Figure Legend from Amplification of the MET Receptor Drives Resistance to Anti-EGFR Therapies in Colorectal Cancer
38. Data from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation
39. Data from Amplification of the MET Receptor Drives Resistance to Anti-EGFR Therapies in Colorectal Cancer
40. 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
41. 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
42. Supplementary Information 1 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation
43. Supplementary Data 3 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation
44. Supplementary Data 1 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation
45. Supplementary Figure 3 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
46. 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
47. Supplementary Figures S1-S6 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
48. 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
49. Supplementary Figure Legends 1-7 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer
50. Supplementary Figure 2 from Inhibition of MEK and PI3K/mTOR Suppresses Tumor Growth but Does Not Cause Tumor Regression in Patient-Derived Xenografts of RAS-Mutant Colorectal Carcinomas
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