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1. Supplementary Tables S1-S2 from Sex-Biased T-cell Exhaustion Drives Differential Immune Responses in Glioblastoma

2. Supplementary Figures S1-S16 from Sex-Biased T-cell Exhaustion Drives Differential Immune Responses in Glioblastoma

3. Data from Sex-Biased T-cell Exhaustion Drives Differential Immune Responses in Glioblastoma

4. Sex-Biased T-cell Exhaustion Drives Differential Immune Responses in Glioblastoma

5. Correction: Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets

6. Supplementary Data from Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets

7. Supplementary Figures from Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets

8. Data from Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets

9. Supplementary Data from MECP2 Is a Frequently Amplified Oncogene with a Novel Epigenetic Mechanism That Mimics the Role of Activated RAS in Malignancy

10. Supplementary Figures S1 - S6 from MECP2 Is a Frequently Amplified Oncogene with a Novel Epigenetic Mechanism That Mimics the Role of Activated RAS in Malignancy

11. Data from Telomeric Allelic Imbalance Indicates Defective DNA Repair and Sensitivity to DNA-Damaging Agents

12. Data from Myeloid-Derived Suppressor Cell Subsets Drive Glioblastoma Growth in a Sex-Specific Manner

13. Supplementary Methods from MECP2 Is a Frequently Amplified Oncogene with a Novel Epigenetic Mechanism That Mimics the Role of Activated RAS in Malignancy

14. Supplementary Table 1 from Myeloid-Derived Suppressor Cell Subsets Drive Glioblastoma Growth in a Sex-Specific Manner

15. Data from ADAMDEC1 Maintains a Growth Factor Signaling Loop in Cancer Stem Cells

16. Data from MECP2 Is a Frequently Amplified Oncogene with a Novel Epigenetic Mechanism That Mimics the Role of Activated RAS in Malignancy

17. Figure S6 from ADAMDEC1 Maintains a Growth Factor Signaling Loop in Cancer Stem Cells

18. Table S1 from ADAMDEC1 Maintains a Growth Factor Signaling Loop in Cancer Stem Cells

19. Supplementary Methods from Telomeric Allelic Imbalance Indicates Defective DNA Repair and Sensitivity to DNA-Damaging Agents

20. Supplementary Figures 1-7 from Telomeric Allelic Imbalance Indicates Defective DNA Repair and Sensitivity to DNA-Damaging Agents

21. Supplementary Figures from Myeloid-Derived Suppressor Cell Subsets Drive Glioblastoma Growth in a Sex-Specific Manner

22. Supplementary Legends_qc from Functional Subclone Profiling for Prediction of Treatment-Induced Intratumor Population Shifts and Discovery of Rational Drug Combinations in Human Glioblastoma

23. Supplementary Figure S5 from Pharmacological Targeting of the Histone Chaperone Complex FACT Preferentially Eliminates Glioblastoma Stem Cells and Prolongs Survival in Preclinical Models

24. Supplementary Data from VRK1 Is a Synthetic–Lethal Target in VRK2-Deficient Glioblastoma

25. Data from Pharmacological Targeting of the Histone Chaperone Complex FACT Preferentially Eliminates Glioblastoma Stem Cells and Prolongs Survival in Preclinical Models

26. Supplementary Tables S1qc-S3qc from Functional Subclone Profiling for Prediction of Treatment-Induced Intratumor Population Shifts and Discovery of Rational Drug Combinations in Human Glioblastoma

28. Supplementary Figure from VRK1 Is a Synthetic–Lethal Target in VRK2-Deficient Glioblastoma

29. Supplemental Figure Legends from Pharmacological Targeting of the Histone Chaperone Complex FACT Preferentially Eliminates Glioblastoma Stem Cells and Prolongs Survival in Preclinical Models

30. Data from New Advances and Challenges of Targeting Cancer Stem Cells

31. Supplementary Figure S5qc from Functional Subclone Profiling for Prediction of Treatment-Induced Intratumor Population Shifts and Discovery of Rational Drug Combinations in Human Glioblastoma

32. CSC 2016 conference program from New Advances and Challenges of Targeting Cancer Stem Cells

33. Supplementary Figures S3qc and S4qc from Functional Subclone Profiling for Prediction of Treatment-Induced Intratumor Population Shifts and Discovery of Rational Drug Combinations in Human Glioblastoma

34. Supplementary Methods, Supplementary Figures 1-4, Supplementary Tables 1-6 from Homologous Recombination Deficiency (HRD) Score Predicts Response to Platinum-Containing Neoadjuvant Chemotherapy in Patients with Triple-Negative Breast Cancer

35. Supplemental Materials & Methods from Pharmacological Targeting of the Histone Chaperone Complex FACT Preferentially Eliminates Glioblastoma Stem Cells and Prolongs Survival in Preclinical Models

36. Data from VRK1 Is a Synthetic–Lethal Target in VRK2-Deficient Glioblastoma

37. Abstract P5-06-05: Whole-genome bisulfite sequencing of single circulating tumor cells identifies cellular methylation heterogeneity in metastatic breast cancer

38. Abstract P5-06-02: Circulating tumor cells in metastatic breast cancer highlight potential role of copy number evolution in late-stage cancer mutational profile

39. Distinct Cell Adhesion Signature Defines Glioblastoma Myeloid-Derived Suppressor Cell Subsets

40. VRK1 Is a Synthetic–Lethal Target in VRK2-Deficient Glioblastoma

42. Myeloid-Derived Suppressor Cell Subsets Drive Glioblastoma Growth in a Sex-Specific Manner

43. Association of Tumor-Infiltrating Lymphocytes with Homologous Recombination Deficiency and BRCA1/2 Status in Patients with Early Triple-Negative Breast Cancer: A Pooled Analysis

44. Abstract OT2-03-02: A pilot trial of hyperthermia in combination with olaparib in breast cancer patients with chest wall recurrences

45. ADAMDEC1 Maintains a Growth Factor Signaling Loop in Cancer Stem Cells

46. New Advances and Challenges of Targeting Cancer Stem Cells

47. Functional Subclone Profiling for Prediction of Treatment-Induced Intratumor Population Shifts and Discovery of Rational Drug Combinations in Human Glioblastoma

48. Homologous Recombination Deficiency (HRD) Score Predicts Response to Platinum-Containing Neoadjuvant Chemotherapy in Patients with Triple-Negative Breast Cancer

49. Pharmacological Targeting of the Histone Chaperone Complex FACT Preferentially Eliminates Glioblastoma Stem Cells and Prolongs Survival in Preclinical Models

50. MECP2 Is a Frequently Amplified Oncogene with a Novel Epigenetic Mechanism That Mimics the Role of Activated RAS in Malignancy

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