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1. The BRD4-NUT fusion alone drives malignant transformation of NUT carcinoma

2. EZH2 Cooperates with BRD4-NUT to Drive NUT Carcinoma Growth by Silencing Key Tumor Suppressor Genes

3. Supplementary Appendix S1 from Phase I trial of Ganitumab plus Dasatinib to Cotarget the Insulin-Like Growth Factor 1 Receptor and Src Family Kinase YES in Rhabdomyosarcoma

4. Supplementary Dataset S1 from Phase I trial of Ganitumab plus Dasatinib to Cotarget the Insulin-Like Growth Factor 1 Receptor and Src Family Kinase YES in Rhabdomyosarcoma

5. Supplementary Table S5 from Phase I trial of Ganitumab plus Dasatinib to Cotarget the Insulin-Like Growth Factor 1 Receptor and Src Family Kinase YES in Rhabdomyosarcoma

6. Supplementary Figure S2 from Phase I trial of Ganitumab plus Dasatinib to Cotarget the Insulin-Like Growth Factor 1 Receptor and Src Family Kinase YES in Rhabdomyosarcoma

7. Data from Phase I trial of Ganitumab plus Dasatinib to Cotarget the Insulin-Like Growth Factor 1 Receptor and Src Family Kinase YES in Rhabdomyosarcoma

8. Abstract P2-11-06: Plasma assay of methylated DNA markers (MDM) detects patients with metastatic breast cancer (MBC) compared to healthy controls and treated breast cancer patients with no evidence of disease

9. Genomic Patterns of Malignant Peripheral Nerve Sheath Tumor (MPNST) Evolution Correlate with Clinical Outcome and Are Detectable in Cell-Free DNA

10. Phase I trial of Ganitumab plus Dasatinib to Cotarget the Insulin-Like Growth Factor 1 Receptor and Src Family Kinase YES in Rhabdomyosarcoma

11. A Phase II Trial of Guadecitabine in Children and Adults with SDH-Deficient GIST, Pheochromocytoma, Paraganglioma, and HLRCC-Associated Renal Cell Carcinoma

12. Data from Genomic Patterns of Malignant Peripheral Nerve Sheath Tumor (MPNST) Evolution Correlate with Clinical Outcome and Are Detectable in Cell-Free DNA

13. Supplementary Figures 1-15 from Genomic Patterns of Malignant Peripheral Nerve Sheath Tumor (MPNST) Evolution Correlate with Clinical Outcome and Are Detectable in Cell-Free DNA

14. Abstract 2219: Urine cell-free DNA multi-omics to detect molecular residual disease and predict survival in bladder cancer patients

15. Supplementary Tables S1 and S2 from Genomic Patterns of Malignant Peripheral Nerve Sheath Tumor (MPNST) Evolution Correlate with Clinical Outcome and Are Detectable in Cell-Free DNA

16. Table S3 from Induction of Thioredoxin-Interacting Protein by a Histone Deacetylase Inhibitor, Entinostat, Is Associated with DNA Damage and Apoptosis in Esophageal Adenocarcinoma

17. Tables S1 and S2 from Induction of Thioredoxin-Interacting Protein by a Histone Deacetylase Inhibitor, Entinostat, Is Associated with DNA Damage and Apoptosis in Esophageal Adenocarcinoma

18. Supplemental Figures 1-15 from Induction of Thioredoxin-Interacting Protein by a Histone Deacetylase Inhibitor, Entinostat, Is Associated with DNA Damage and Apoptosis in Esophageal Adenocarcinoma

19. Data from Induction of Thioredoxin-Interacting Protein by a Histone Deacetylase Inhibitor, Entinostat, Is Associated with DNA Damage and Apoptosis in Esophageal Adenocarcinoma

20. Supplementary Table S3 from A Phase II Window of Opportunity Study of Neoadjuvant PD-L1 versus PD-L1 plus CTLA-4 Blockade for Patients with Malignant Pleural Mesothelioma

21. Supplementary Appendix S1 from A Phase II Trial of Guadecitabine in Children and Adults with SDH-Deficient GIST, Pheochromocytoma, Paraganglioma, and HLRCC-Associated Renal Cell Carcinoma

22. Supplementary Figure S5 from A Phase II Window of Opportunity Study of Neoadjuvant PD-L1 versus PD-L1 plus CTLA-4 Blockade for Patients with Malignant Pleural Mesothelioma

23. Supplementary Methods S1 from A Phase II Window of Opportunity Study of Neoadjuvant PD-L1 versus PD-L1 plus CTLA-4 Blockade for Patients with Malignant Pleural Mesothelioma

24. Supplementary Table S2 from A Phase II Trial of Guadecitabine in Children and Adults with SDH-Deficient GIST, Pheochromocytoma, Paraganglioma, and HLRCC-Associated Renal Cell Carcinoma

25. Supplementary Figure 2 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

26. Supplementary Table 6 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

27. Supplementary Figure S5 from Mithramycin Depletes Specificity Protein 1 and Activates p53 to Mediate Senescence and Apoptosis of Malignant Pleural Mesothelioma Cells

28. Supplementary Data from Therapeutic Targeting of Macrophage Plasticity Remodels the Tumor-Immune Microenvironment

29. Supplementary Table S1 from Mithramycin Depletes Specificity Protein 1 and Activates p53 to Mediate Senescence and Apoptosis of Malignant Pleural Mesothelioma Cells

30. Supplementary Table 1 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

31. Supplementary Figure 4 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

32. Supplementary Materials and Methods from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

33. Supplementary Figure 6 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

34. Supplementary Figure 3 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

35. Supplementary Table 5 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

36. Supplementary Figure 1 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

37. Supplementary Table 2 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

38. Supplementary Table 3 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

39. Supplementary Figure 5 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

40. Supplementary Table 4 from Polycomb Repressor Complex-2 Is a Novel Target for Mesothelioma Therapy

41. Supplementary Methods from Mithramycin Depletes Specificity Protein 1 and Activates p53 to Mediate Senescence and Apoptosis of Malignant Pleural Mesothelioma Cells

42. Supplementary Table 2 from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

43. Supplementary Table 3 from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

44. Supplementary Figure 4 from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

45. Data from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

46. Supplementary Figure 3 from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

47. Supplementary Table 1 from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

48. Supplementary Figure 2 from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

49. Supplementary Methods from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

50. Supplementary Figure 1 from Mithramycin Represses Basal and Cigarette Smoke–Induced Expression of ABCG2 and Inhibits Stem Cell Signaling in Lung and Esophageal Cancer Cells

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