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2. Impaired proteolysis of non-canonical RAS proteins drives clonal hematopoietic transformation

3. Concurrent SOS1 and MEK suppression inhibits signaling and growth of NF1-null melanoma

4. ARAF protein kinase activates RAS by antagonizing its binding to RASGAP NF1

5. The sixth international RASopathies symposium: Precision medicine-From promise to practice.

6. Anatomic position determines oncogenic specificity in melanoma

7. eIF4A controls translation of estrogen receptor alpha and is a therapeutic target in advanced breast cancer

8. A next-generation BRAF inhibitor overcomes resistance to BRAF inhibition in patients with BRAF-mutant cancers using pharmacokinetics-informed dose escalation

9. Selective inhibitors of mTORC1 activate 4EBP1 and suppress tumor growth

13. Anti-tumor effects of an ID antagonist with no observed acquired resistance

16. AXL Mediates Resistance to PI3Kα Inhibition by Activating the EGFR/PKC/mTOR Axis in Head and Neck and Esophageal Squamous Cell Carcinomas

18. Loss of NF1 in Cutaneous Melanoma Is Associated with RAS Activation and MEK Dependence

19. ERK Activation by BRAFV600E suppresses mesenchymal migration and tumorigenesis by inhibiting RAC1.

20. Efficacy of MEK inhibition in patients with histiocytic neoplasms

22. RAF inhibitor resistance is mediated by dimerization of aberrantly spliced BRAF(V600E)

23. RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF

24. Supplementary Table 1 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

25. Supplementary Table 2 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

26. Supplementary Figure 6 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

27. Supplementary Figure 3 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

28. Supplementary Figure 4 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

29. Supplementary Figure 5 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

30. Supplementary Figure 1 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

31. Supplementary Figure 2 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

34. Author Correction: Selective inhibitors of mTORC1 activate 4EBP1 and suppress tumor growth

37. Abstract 2: Vertical MAPK pathway targeting in novel genetically engineered mouse and cell line models of NF1-altered melanoma: the mSK-Mel murine cohort

38. Supplementary Table 3 from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

40. Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

41. Data from Molecular Characterization of Acquired Resistance to KRASG12C–EGFR Inhibition in Colorectal Cancer

42. Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation

44. Data from Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms

46. 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

47. Supplementary Table 2 from Prospective Blinded Study of BRAFV600E Mutation Detection in Cell-Free DNA of Patients with Systemic Histiocytic Disorders

48. Data from V211D Mutation in MEK1 Causes Resistance to MEK Inhibitors in Colon Cancer

49. Supplementary Figure 3 from EGFR Blockade Reverts Resistance to KRASG12C Inhibition in Colorectal Cancer

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