111 results on '"Sanson, Marc"'
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2. Supplementary Figure S1. from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
3. Supplementary Figure S7 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
4. Supplementary Figure S3 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
5. Supplementary Figure S2 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
6. Supplementary Figure S5 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
7. Supplementary Figure S4 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
8. Supplementary Tables S1-S3 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
9. Supplementary Figure S3 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
10. Data from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
11. Supplementary Figure S2 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
12. Data from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
13. Supplementary Figure S1. from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
14. Supplementary Figure S6 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
15. Supplementary Figure S5 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
16. Supplementary Figure S7 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
17. Supplementary Figure S8 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
18. Supplementary Figure S6 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
19. Supplementary Figure S4 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
20. Supplementary Figure S8 from LZTR1 Mutation Mediates Oncogenesis through Stabilization of EGFR and AXL
21. Supplementary Methods, Tables, and Figure from Futibatinib, an Irreversible FGFR1–4 Inhibitor, in Patients with Advanced Solid Tumors Harboring FGF/FGFR Aberrations: A Phase I Dose-Expansion Study
22. Data from Futibatinib, an Irreversible FGFR1–4 Inhibitor, in Patients with Advanced Solid Tumors Harboring FGF/FGFR Aberrations: A Phase I Dose-Expansion Study
23. Supplementary Methods, Tables, and Figure from Futibatinib, an Irreversible FGFR1–4 Inhibitor, in Patients with Advanced Solid Tumors Harboring FGF/FGFR Aberrations: A Phase I Dose-Expansion Study
24. Data from Futibatinib, an Irreversible FGFR1–4 Inhibitor, in Patients with Advanced Solid Tumors Harboring FGF/FGFR Aberrations: A Phase I Dose-Expansion Study
25. S1: Genetic landscape of MDM2/TP53 pathway. from Preclinical Efficacy of the MDM2 Inhibitor RG7112 in MDM2-Amplified and TP53 Wild-type Glioblastomas
26. S7: Additional material and methods from Preclinical Efficacy of the MDM2 Inhibitor RG7112 in MDM2-Amplified and TP53 Wild-type Glioblastomas
27. Supplementary Table 7 from Transcriptome-Wide Association Study Identifies New Candidate Susceptibility Genes for Glioma
28. Figure S2 from Everolimus and Octreotide for Patients with Recurrent Meningioma: Results from the Phase II CEVOREM Trial
29. Supplementary Figure from Temozolomide and Radiotherapy versus Radiotherapy Alone in Patients with Glioblastoma, IDH-wildtype: Post Hoc Analysis of the EORTC Randomized Phase III CATNON Trial
30. Supplementary Figure 5 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma
31. S5: MDM2, MDM4 and TP53 gene expression in the GBM cell lines of cohort #1 as determined by RT-qPCR. from Preclinical Efficacy of the MDM2 Inhibitor RG7112 in MDM2-Amplified and TP53 Wild-type Glioblastomas
32. Figure S1 from Everolimus and Octreotide for Patients with Recurrent Meningioma: Results from the Phase II CEVOREM Trial
33. Supplementary Figure from Temozolomide and Radiotherapy versus Radiotherapy Alone in Patients with Glioblastoma, IDH-wildtype: Post Hoc Analysis of the EORTC Randomized Phase III CATNON Trial
34. Supplementary Figure from Temozolomide and Radiotherapy versus Radiotherapy Alone in Patients with Glioblastoma, IDH-wildtype: Post Hoc Analysis of the EORTC Randomized Phase III CATNON Trial
35. Supplementary Table 5 from A Hypermethylated Phenotype Is a Better Predictor of Survival than MGMT Methylation in Anaplastic Oligodendroglial Brain Tumors: A Report from EORTC Study 26951
36. Supplementary Figure Legend from A Hypermethylated Phenotype Is a Better Predictor of Survival than MGMT Methylation in Anaplastic Oligodendroglial Brain Tumors: A Report from EORTC Study 26951
37. Supplementary Figure 2 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma
38. Supplementary Table 5 from A Hypermethylated Phenotype Is a Better Predictor of Survival than MGMT Methylation in Anaplastic Oligodendroglial Brain Tumors: A Report from EORTC Study 26951
39. S3: Evolution of MDM2 and TP53 status over time of 5 patients affected by MDM2-amplified GBM. from Preclinical Efficacy of the MDM2 Inhibitor RG7112 in MDM2-Amplified and TP53 Wild-type Glioblastomas
40. Figure S3 from Everolimus and Octreotide for Patients with Recurrent Meningioma: Results from the Phase II CEVOREM Trial
41. Supplementary Figure from Temozolomide and Radiotherapy versus Radiotherapy Alone in Patients with Glioblastoma, IDH-wildtype: Post Hoc Analysis of the EORTC Randomized Phase III CATNON Trial
42. Supplementary Figure 1 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma
43. Figure S2 from Everolimus and Octreotide for Patients with Recurrent Meningioma: Results from the Phase II CEVOREM Trial
44. Supplementary Tables from Safety and Feasibility of Repeated and Transient Blood–Brain Barrier Disruption by Pulsed Ultrasound in Patients with Recurrent Glioblastoma
45. Data from Transcriptome-Wide Association Study Identifies New Candidate Susceptibility Genes for Glioma
46. Table S2 from Everolimus and Octreotide for Patients with Recurrent Meningioma: Results from the Phase II CEVOREM Trial
47. S7: Additional material and methods from Preclinical Efficacy of the MDM2 Inhibitor RG7112 in MDM2-Amplified and TP53 Wild-type Glioblastomas
48. Supplementary Figure 6 from Detection, Characterization, and Inhibition of FGFR–TACC Fusions in IDH Wild-type Glioma
49. Supplementary Figure 3 from A Hypermethylated Phenotype Is a Better Predictor of Survival than MGMT Methylation in Anaplastic Oligodendroglial Brain Tumors: A Report from EORTC Study 26951
50. Data from A Hypermethylated Phenotype Is a Better Predictor of Survival than MGMT Methylation in Anaplastic Oligodendroglial Brain Tumors: A Report from EORTC Study 26951
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