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3. Coexisting cancer stem cells with heterogeneous gene amplifications, transcriptional profiles, and malignancy are isolated from single glioblastomas

14. MET Oncogene Enhances Pro-Migratory Functions by Counteracting NMDAR2B Cleavage.

15. Supplementary Figure S2 from Amplification of the MET Receptor Drives Resistance to Anti-EGFR Therapies in Colorectal Cancer

16. Supplementary Data 2 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation

17. 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

18. 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

19. 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

20. 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

21. 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

22. 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

23. 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

24. 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

25. 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

26. Data 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 4 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 Legend from Amplification of the MET Receptor Drives Resistance to Anti-EGFR Therapies in Colorectal Cancer

29. Data from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation

30. Data from Amplification of the MET Receptor Drives Resistance to Anti-EGFR Therapies in Colorectal Cancer

31. 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

32. 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

33. Supplementary Information 1 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation

34. Supplementary Data 3 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation

35. Supplementary Data 1 from Liquid Biopsy of Cerebrospinal Fluid Enables Selective Profiling of Glioma Molecular Subtypes at First Clinical Presentation

36. Supplementary Figure 3 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer

37. 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

38. 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

39. 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

40. Supplementary Figure Legends 1-7 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer

41. 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

42. SupplementaryTable 1 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

43. SupplementaryTable 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

44. Supplementary Figure 3 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

45. Supplementary Figure 2 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer

47. Supplementary Figure 5 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer

48. Supplementary Figure 1 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

49. Supplementary Figure 6 from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer

50. Supplementary Materials and Methods from MiR-1 Downregulation Cooperates with MACC1 in Promoting MET Overexpression in Human Colon Cancer

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