550 results on '"Yelensky, Roman"'
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2. Rucaparib in relapsed, platinum-sensitive high-grade ovarian carcinoma (ARIEL2 Part 1): an international, multicentre, open-label, phase 2 trial
3. Presence of both alterations in FGFR/FGF and PI3K/AKT/mTOR confer improved outcomes for patients with metastatic breast cancer treated with PI3K/AKT/mTOR inhibitors
4. Multiple gene aberrations and breast cancer: lessons from super-responders
5. Next generation sequencing of exceptional responders with BRAF-mutant melanoma: implications for sensitivity and resistance
6. Anastrozole and everolimus in advanced gynecologic and breast malignancies: activity and molecular alterations in the PI3K/AKT/mTOR pathway
7. Unique molecular signatures as a hallmark of patients with metastatic breast cancer: Implications for current treatment paradigms
8. Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
9. Kinase fusions are frequent in Spitz tumours and spitzoid melanomas
10. Update on Tumor Neoantigens and Their Utility: Why It Is Good to Be Different
11. Deep learning using tumor HLA peptide mass spectrometry datasets improves neoantigen identification
12. Data from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
13. Data from RICTOR Amplification Defines a Novel Subset of Patients with Lung Cancer Who May Benefit from Treatment with mTORC1/2 Inhibitors
14. Data from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
15. Data from Triple-Negative Breast Cancer Patients Treated at MD Anderson Cancer Center in Phase I Trials: Improved Outcomes with Combination Chemotherapy and Targeted Agents
16. Supplementary Methods from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
17. Supplementary Table S3 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
18. Supplementary Table S2 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
19. Supplementary Data Figure 5 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
20. Data from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
21. Supplementary Table S1 from TP53 Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics
22. Supplementary Figure S2 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
23. Supplementary Table 4 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
24. Supplementary Table 5 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
25. Supplementary Data Tables from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
26. Supplementary Figure 1 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
27. Supplementary Data Figure 6 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
28. Supplementary Data Figure 7 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
29. Supplementary Data Figure 2 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
30. Supplementary Table S1A - S1B from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
31. Supplementary Data Figure 4 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
32. Supplementary Table 1 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
33. Supplementary Table S1 from Triple-Negative Breast Cancer Patients Treated at MD Anderson Cancer Center in Phase I Trials: Improved Outcomes with Combination Chemotherapy and Targeted Agents
34. Supplementary Data Figure Legends from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
35. Data from TP53 Alterations Correlate with Response to VEGF/VEGFR Inhibitors: Implications for Targeted Therapeutics
36. Data from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
37. Suplpementary Table 2 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
38. Supplementary Figures 1 - 3 from RICTOR Amplification Defines a Novel Subset of Patients with Lung Cancer Who May Benefit from Treatment with mTORC1/2 Inhibitors
39. Supplementary Data Figure 3 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
40. Supplementary Data Figure 1 from Molecular Profiling of the Residual Disease of Triple-Negative Breast Cancers after Neoadjuvant Chemotherapy Identifies Actionable Therapeutic Targets
41. Supplementary Table 3 from Concordance of Genomic Alterations between Primary and Recurrent Breast Cancer
42. Supplementary Patient Data from Emergence of Constitutively Active Estrogen Receptor-α Mutations in Pretreated Advanced Estrogen Receptor–Positive Breast Cancer
43. Supplemental table 1 from Profiling of 149 Salivary Duct Carcinomas, Carcinoma Ex Pleomorphic Adenomas, and Adenocarcinomas, Not Otherwise Specified Reveals Actionable Genomic Alterations
44. Supplementary Table 1 from A High Frequency of Activating Extracellular Domain ERBB2 (HER2) Mutation in Micropapillary Urothelial Carcinoma
45. Data from Cancer Therapy Directed by Comprehensive Genomic Profiling: A Single Center Study
46. Supplementary Table S1: from Cancer Therapy Directed by Comprehensive Genomic Profiling: A Single Center Study
47. Supplemental Figures from RAS/MAPK Activation Is Associated with Reduced Tumor-Infiltrating Lymphocytes in Triple-Negative Breast Cancer: Therapeutic Cooperation Between MEK and PD-1/PD-L1 Immune Checkpoint Inhibitors
48. Supplementary Table S1. from Relapsed Classic E-Cadherin (CDH1)–Mutated Invasive Lobular Breast Cancer Shows a High Frequency of HER2 (ERBB2) Gene Mutations
49. Supplementary Data from Relapsed Classic E-Cadherin (CDH1)–Mutated Invasive Lobular Breast Cancer Shows a High Frequency of HER2 (ERBB2) Gene Mutations
50. Supplementary figure legend from RAS/MAPK Activation Is Associated with Reduced Tumor-Infiltrating Lymphocytes in Triple-Negative Breast Cancer: Therapeutic Cooperation Between MEK and PD-1/PD-L1 Immune Checkpoint Inhibitors
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