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1. DNA demethylation triggers cell free DNA release in colorectal cancer cells

2. Post-surgery sequelae unrelated to disease progression and chemotherapy revealed in follow-up of patients with stage III colon cancer

3. Concurrent RB1 and P53 pathway disruption predisposes to the development of a primitive neuronal component in high-grade gliomas depending on MYC-driven EBF3 transcription

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

6. Circulating tumor DNA to guide rechallenge with panitumumab in metastatic colorectal cancer: the phase 2 CHRONOS trial

8. Liquid Biopsy and Challenge of Assay Heterogeneity for Minimal Residual Disease Assessment in Colon Cancer Treatment.

10. Mutational Signatures in Colorectal Cancer: Translational Insights, Clinical Applications, and Limitations.

11. Transcriptome‐wide gene expression outlier analysis pinpoints therapeutic vulnerabilities in colorectal cancer

12. Adaptive mutability of colorectal cancers in response to targeted therapies

13. A Genomic Analysis Workflow for Colorectal Cancer Precision Oncology

15. Radiologic and Genomic Evolution of Individual Metastases during HER2 Blockade in Colorectal Cancer

18. Abstract LB058: A transcriptome-wide gene expression outlier analysis pinpoints therapeutic vulnerabilities in colorectal cancer

19. Data from Temozolomide Treatment Alters Mismatch Repair and Boosts Mutational Burden in Tumor and Blood of Colorectal Cancer Patients

21. Supplementary Figure from Temozolomide Treatment Alters Mismatch Repair and Boosts Mutational Burden in Tumor and Blood of Colorectal Cancer Patients

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

23. Data from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

24. Supplementary Figure 4 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

25. Supplementary Figure 5 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

26. Data from Acquired Resistance to the TRK Inhibitor Entrectinib in Colorectal Cancer

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

28. Supplementary Figure 1 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

29. Supplementary Table 1 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

30. Supplementary Figure 3 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

31. Supplementary Methods, Figure Legends, Table Legends, Figures S1 - S4, Tables S1 - S5 from Acquired Resistance to the TRK Inhibitor Entrectinib in Colorectal Cancer

32. Data from Tumor Heterogeneity and Lesion-Specific Response to Targeted Therapy in 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 Figures S1 - S3, Tables S1 - S6 from Tumor Heterogeneity and Lesion-Specific Response to Targeted Therapy in Colorectal Cancer

36. Supplementary Figure 2 from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

37. Cell Model Network-UK from Werner Helicase Is a Synthetic-Lethal Vulnerability in Mismatch Repair–Deficient Colorectal Cancer Refractory to Targeted Therapies, Chemotherapy, and Immunotherapy

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

39. Supplementary Figure S3 from Emergence of Multiple EGFR Extracellular Mutations during Cetuximab Treatment in Colorectal Cancer

40. Supplementary Figure Legends from Molecular Landscape of Acquired Resistance to Targeted Therapy Combinations in BRAF-Mutant Colorectal Cancer

41. Supplementary Materials and Methods from Molecular Landscape of Acquired Resistance to Targeted Therapy Combinations in BRAF-Mutant Colorectal Cancer

42. Data from Molecular Landscape of Acquired Resistance to Targeted Therapy Combinations in BRAF-Mutant Colorectal Cancer

43. Supplementary Figures and Tables from Molecular Landscape of Acquired Resistance to Targeted Therapy Combinations in BRAF-Mutant Colorectal Cancer

44. Supplementary Table S3 from Emergence of Multiple EGFR Extracellular Mutations during Cetuximab Treatment in Colorectal Cancer

45. Supplementary Table and Figure Legends from Emergence of Multiple EGFR Extracellular Mutations during Cetuximab Treatment in Colorectal Cancer

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

47. Case report: Preclinical efficacy of NEDD8 and proteasome inhibitors in patient-derived models of signet ring high-grade mucinous colorectal cancer from a Lynch syndrome patient

49. DNA damage response and repair genes in advanced bone and soft tissue sarcomas: An 8-gene signature as a candidate predictive biomarker of response to trabectedin and olaparib combination

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