521 results on '"Halaban, Ruth"'
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2. Unannotated microprotein EMBOW regulates the interactome and chromatin and mitotic functions of WDR5
3. A plasma-based proteomic platform for predicting clinical benefit from immune checkpoint inhibitors in multiple cancers.
4. Clonal determinants of organotropism and survival in metastatic uveal melanoma
5. Dynamic changes of circulating soluble PD-1/PD-L1 and its association with patient survival in immune checkpoint blockade-treated melanoma
6. Circulating Tumor Reactive KIR+CD8+ T cells Suppress Anti-Tumor Immunity in Patients with Melanoma
7. Author Correction: Integrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis
8. Integrative molecular and clinical profiling of acral melanoma links focal amplification of 22q11.21 to metastasis
9. T cell characteristics associated with toxicity to immune checkpoint blockade in patients with melanoma
10. Ultra-sensitive molecular residual disease detection through whole genome sequencing with single-read error correction
11. Future perspectives in melanoma research: meeting report from the "Melanoma Bridge", Napoli, December 5th-8th 2013
12. CD4 T cells and toxicity from immune checkpoint blockade
13. Future Perspectives in melanoma research:Meeting report from the "Melanoma Research: a bridge Naples-USA. Naples, December 6th-7th 2010".
14. Abstract 6670: Association between circulating CD4 memory T cell levels and severe immune-related adverse events in melanoma patients treated with immune checkpoint blockade
15. Supplementary Figure 6 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
16. Supplementary Figure 4 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
17. Supplementary Tables 1-3 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
18. Supplementary Figure 3 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
19. Supplementary Figure 1 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
20. Supplementary Figure 2 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
21. Supplementary Figure 1 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
22. Supplementary Table 4 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
23. Data from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
24. Data from A Serum Protein Signature Associated with Outcome after Anti–PD-1 Therapy in Metastatic Melanoma
25. Supplementary Table 5 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
26. Data from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
27. Supplemental Material, Supplementary Figures 1 and 2, Supplemental Tables 1 - 8 from A Serum Protein Signature Associated with Outcome after Anti–PD-1 Therapy in Metastatic Melanoma
28. Supplementary Figure 5 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
29. Supplementary Table 6 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
30. Supplementary Figure 7 from Preexisting MEK1 Exon 3 Mutations in V600E/KBRAF Melanomas Do Not Confer Resistance to BRAF Inhibitors
31. Supplementary Table Legends 1-6, Figure Legend 1 from Phosphoproteomic Screen Identifies Potential Therapeutic Targets in Melanoma
32. Supplementary Figure S2 from PLEKHA5 as a Biomarker and Potential Mediator of Melanoma Brain Metastasis
33. Supplementary Figure Legends from PLEKHA5 as a Biomarker and Potential Mediator of Melanoma Brain Metastasis
34. Supplementary Table S3 from PLEKHA5 as a Biomarker and Potential Mediator of Melanoma Brain Metastasis
35. Supplementary Figures S1-S5 from Plasma Markers for Identifying Patients with Metastatic Melanoma
36. Supplementary Materials and Methods from PLEKHA5 as a Biomarker and Potential Mediator of Melanoma Brain Metastasis
37. Supplementary Table 3 from Expression Profiling Reveals Novel Pathways in the Transformation of Melanocytes to Melanomas
38. Supplementary Table S2 from PDK1 and SGK3 Contribute to the Growth of BRAF-Mutant Melanomas and Are Potential Therapeutic Targets
39. Data from PDK1 and SGK3 Contribute to the Growth of BRAF-Mutant Melanomas and Are Potential Therapeutic Targets
40. Supplementary Table 1 from Expression Profiling Reveals Novel Pathways in the Transformation of Melanocytes to Melanomas
41. Supplementary Figures S1-S6 from PDK1 and SGK3 Contribute to the Growth of BRAF-Mutant Melanomas and Are Potential Therapeutic Targets
42. Supplementary Table 2 from Expression Profiling Reveals Novel Pathways in the Transformation of Melanocytes to Melanomas
43. Supplementary Table and Figure Legends from PDK1 and SGK3 Contribute to the Growth of BRAF-Mutant Melanomas and Are Potential Therapeutic Targets
44. Integrative analysis of epigenetic modulation in melanoma cell response to decitabine: clinical implications.
45. Spitz nevi and Spitzoid melanomas: exome sequencing and comparison with conventional melanocytic nevi and melanomas
46. Endoplasmic Reticulum Retention Is a Common Defect Associated with Tyrosinase-Negative Albinism
47. Identification of Morc (Microrchidia), a Mutation that Results in Arrest of Spermatogenesis at an Early Meiotic Stage in the Mouse
48. Early B cell changes predict autoimmunity following combination immune checkpoint blockade
49. Chymase Cleavage of Stem Cell Factor Yields a Bioactive, Soluble Product
50. Aberrant Retention of Tyrosinase in the Endoplasmic Reticulum Mediates Accelerated Degradation of the Enzyme and Contributes to the Dedifferentiated Phenotype of Amelanotic Melanoma Cells
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