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5. Data from ERK Inhibition Overcomes Acquired Resistance to MEK Inhibitors

6. Supplementary Table S1 from Genetic Alterations and Oncogenic Pathways Associated with Breast Cancer Subtypes

7. Supplementary Figures 1-7, Methods from ERK Inhibition Overcomes Acquired Resistance to MEK Inhibitors

8. Supplementary Methods, Figures 1-4 from PPM1H Is a p27 Phosphatase Implicated in Trastuzumab Resistance

10. Data from PPM1H Is a p27 Phosphatase Implicated in Trastuzumab Resistance

11. Supplementary Figures S1-S4 from Genetic Alterations and Oncogenic Pathways Associated with Breast Cancer Subtypes

12. Supplementary Table 2 from Phosphoinositide 3-Kinase (PI3K) Pathway Alterations Are Associated with Histologic Subtypes and Are Predictive of Sensitivity to PI3K Inhibitors in Lung Cancer Preclinical Models

13. Table S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer

14. Data from Suppression of HER2/HER3-Mediated Growth of Breast Cancer Cells with Combinations of GDC-0941 PI3K Inhibitor, Trastuzumab, and Pertuzumab

15. Figure S4 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer

16. Supplementary Figures S1-4 and Tables S1-6 from An Antibody–Drug Conjugate Directed against Lymphocyte Antigen 6 Complex, Locus E (LY6E) Provides Robust Tumor Killing in a Wide Range of Solid Tumor Malignancies

17. Note S1 from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer

18. Supplementary Figure legends from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer

19. Data from Therapeutic Targeting of the CBP/p300 Bromodomain Blocks the Growth of Castration-Resistant Prostate Cancer

20. Supplemental Methods and Figure Legends from An Antibody–Drug Conjugate Directed against Lymphocyte Antigen 6 Complex, Locus E (LY6E) Provides Robust Tumor Killing in a Wide Range of Solid Tumor Malignancies

21. Supplementary Figures 1 - 6 from Phosphoinositide 3-Kinase (PI3K) Pathway Alterations Are Associated with Histologic Subtypes and Are Predictive of Sensitivity to PI3K Inhibitors in Lung Cancer Preclinical Models

22. Supplementary Methods and Tables from Loss of NAPRT1 Expression by Tumor-Specific Promoter Methylation Provides a Novel Predictive Biomarker for NAMPT Inhibitors

23. Supplementary Table 1 from Phosphoinositide 3-Kinase (PI3K) Pathway Alterations Are Associated with Histologic Subtypes and Are Predictive of Sensitivity to PI3K Inhibitors in Lung Cancer Preclinical Models

24. Supplementary Methods from Phosphoinositide 3-Kinase (PI3K) Pathway Alterations Are Associated with Histologic Subtypes and Are Predictive of Sensitivity to PI3K Inhibitors in Lung Cancer Preclinical Models

25. Supplementary Figure 1 from Loss of NAPRT1 Expression by Tumor-Specific Promoter Methylation Provides a Novel Predictive Biomarker for NAMPT Inhibitors

26. Supplementary Data from Suppression of HER2/HER3-Mediated Growth of Breast Cancer Cells with Combinations of GDC-0941 PI3K Inhibitor, Trastuzumab, and Pertuzumab

27. Supplementary Table 3 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

28. Data from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

29. Supplementary Table 7 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

30. Supplementary Table 2 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

31. Supplementary Table 4 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

33. Supplementary Table 5 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

34. Supplementary Table 6 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

35. Supplementary Table 1 from Comparative Oncogenomics Identifies PSMB4 and SHMT2 as Potential Cancer Driver Genes

37. Genomic Analysis of Smoothened Inhibitor Resistance in Basal Cell Carcinoma

38. A transcriptional MAPK Pathway Activity Score (MPAS) is a clinically relevant biomarker in multiple cancer types

39. Reproducible pharmacogenomics profiling of cancer cell line panels

40. Precision Discovery of Novel Inhibitors of Cancer Target HsMetAP1 from Vast Metagenomic Diversity

41. Targeting p21-activated kinase 1 (PAK1) to induce apoptosis of tumor cells

42. Recurrent R-spondin fusions in colon cancer

43. The mutation spectrum revealed by paired genome sequences from a lung cancer patient

44. PAK1 mediates pancreatic cancer cell migration and resistance to MET inhibition

47. Recurrent R-spondin fusions in colon cancer

50. Diverse somatic mutation patterns and pathway alterations in human cancers

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