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1. Ovarian cancer mutational processes drive site-specific immune evasion

2. ACK1 and BRK non-receptor tyrosine kinase deficiencies are associated with familial systemic lupus and involved in efferocytosis

3. Author Correction: FOXA1 repression drives lineage plasticity and immune heterogeneity in bladder cancers with squamous differentiation

4. FOXA1 repression drives lineage plasticity and immune heterogeneity in bladder cancers with squamous differentiation

6. Tumor fraction-guided cell-free DNA profiling in metastatic solid tumor patients

7. NF2 Loss Promotes Oncogenic RAS-Induced Thyroid Cancers via YAP-Dependent Transactivation of RAS Proteins and Sensitizes Them to MEK Inhibition.

8. Hotspot activating PRKD1 somatic mutations in polymorphous low-grade adenocarcinomas of the salivary glands

9. Phase 1b trial of an ibrutinib-based combination therapy in recurrent/refractory CNS lymphoma

10. Supplementary Table S2 from Overcoming Barriers to Tumor Genomic Profiling through Direct-to-Patient Outreach

11. Data from Overcoming Barriers to Tumor Genomic Profiling through Direct-to-Patient Outreach

12. Supplementary Figure S1 from Overcoming Barriers to Tumor Genomic Profiling through Direct-to-Patient Outreach

13. Gene Expression Profiles Accurately Predict Outcome Following Liver Resection in Patients with Metastatic Colorectal Cancer

14. Tumour lineage shapes BRCA-mediated phenotypes

16. Tracking tumour evolution in glioma through liquid biopsies of cerebrospinal fluid

17. Comprehensive genomic characterization of squamous cell lung cancers

18. Stat3 Mediates Expression of Autotaxin in Breast Cancer

20. Subtype-specific genomic alterations define new targets for soft-tissue sarcoma therapy

21. Data from Synthetic Lethality in ATM-Deficient RAD50-Mutant Tumors Underlies Outlier Response to Cancer Therapy

22. Supplementary Figure S5 from Relief of Feedback Inhibition of HER3 Transcription by RAF and MEK Inhibitors Attenuates Their Antitumor Effects in BRAF-Mutant Thyroid Carcinomas

23. Data from Efficacy of Intermittent Combined RAF and MEK Inhibition in a Patient with Concurrent BRAF- and NRAS-Mutant Malignancies

24. Supplementary Figures S1 - S10, Tables S1 - S3 from NF2 Loss Promotes Oncogenic RAS-Induced Thyroid Cancers via YAP-Dependent Transactivation of RAS Proteins and Sensitizes Them to MEK Inhibition

25. Supplementary Methods and References from Relief of Feedback Inhibition of HER3 Transcription by RAF and MEK Inhibitors Attenuates Their Antitumor Effects in BRAF-Mutant Thyroid Carcinomas

26. Supplementary Figures 1 - 10 from Synthetic Lethality in ATM-Deficient RAD50-Mutant Tumors Underlies Outlier Response to Cancer Therapy

27. Supplementary Figures from Isoform Switching as a Mechanism of Acquired Resistance to Mutant Isocitrate Dehydrogenase Inhibition

29. Supplementary Figure 1 from Efficacy of Intermittent Combined RAF and MEK Inhibition in a Patient with Concurrent BRAF- and NRAS-Mutant Malignancies

30. Supplementary Methods, Supplementary Tables 1 through 7, and Supplementary Figures 1 through 7 from Ibrutinib Unmasks Critical Role of Bruton Tyrosine Kinase in Primary CNS Lymphoma

31. Supplementary Figure 2 from Efficacy of Intermittent Combined RAF and MEK Inhibition in a Patient with Concurrent BRAF- and NRAS-Mutant Malignancies

32. Supplementary Materials from Synthetic Lethality in ATM-Deficient RAD50-Mutant Tumors Underlies Outlier Response to Cancer Therapy

33. Data from NF2 Loss Promotes Oncogenic RAS-Induced Thyroid Cancers via YAP-Dependent Transactivation of RAS Proteins and Sensitizes Them to MEK Inhibition

34. Data from Ibrutinib Unmasks Critical Role of Bruton Tyrosine Kinase in Primary CNS Lymphoma

35. Data from Frequent Alterations and Epigenetic Silencing of Differentiation Pathway Genes in Structurally Rearranged Liposarcomas

36. Supplementary Tables and Legend from Efficacy of Intermittent Combined RAF and MEK Inhibition in a Patient with Concurrent BRAF- and NRAS-Mutant Malignancies

37. Supplementary Tables 1 - 6 from Synthetic Lethality in ATM-Deficient RAD50-Mutant Tumors Underlies Outlier Response to Cancer Therapy

38. Supplementary Figure 3 from Efficacy of Intermittent Combined RAF and MEK Inhibition in a Patient with Concurrent BRAF- and NRAS-Mutant Malignancies

39. Supplementary Tables 1-7 from Frequent Alterations and Epigenetic Silencing of Differentiation Pathway Genes in Structurally Rearranged Liposarcomas

40. Supplementary Methods from Isoform Switching as a Mechanism of Acquired Resistance to Mutant Isocitrate Dehydrogenase Inhibition

41. Supplementary Methods, Figures 1-10 from Frequent Alterations and Epigenetic Silencing of Differentiation Pathway Genes in Structurally Rearranged Liposarcomas

42. Supplementary Figure 4 from Efficacy of Intermittent Combined RAF and MEK Inhibition in a Patient with Concurrent BRAF- and NRAS-Mutant Malignancies

43. Supplementary Table S1 from Germline Lysine-Specific Demethylase 1 (LSD1/KDM1A) Mutations Confer Susceptibility to Multiple Myeloma

44. Supplementary Figures 1 - 11, Tables 1 - 2 from Tumor Genetic Analyses of Patients with Metastatic Renal Cell Carcinoma and Extended Benefit from mTOR Inhibitor Therapy

45. Supplementary Tables from A Validated Prognostic Multigene Expression Assay for Overall Survival in Resected Colorectal Cancer Liver Metastases

46. Supplementary Table 4 from Tumor Genetic Analyses of Patients with Metastatic Renal Cell Carcinoma and Extended Benefit from mTOR Inhibitor Therapy

47. Supplementary Table S2 from Lobular Carcinomas In Situ Display Intralesion Genetic Heterogeneity and Clonal Evolution in the Progression to Invasive Lobular Carcinoma

48. Supplementary Data from Coaltered Ras/B-raf and TP53 Is Associated with Extremes of Survivorship and Distinct Patterns of Metastasis in Patients with Metastatic Colorectal Cancer

49. Supplementary Data from Germline Lysine-Specific Demethylase 1 (LSD1/KDM1A) Mutations Confer Susceptibility to Multiple Myeloma

50. Supplementary Figure S2 from Lobular Carcinomas In Situ Display Intralesion Genetic Heterogeneity and Clonal Evolution in the Progression to Invasive Lobular Carcinoma

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