207 results on '"Siraj, M"'
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2. Data from The Genomics of Colorectal Cancer in Populations with African and European Ancestry
3. Abstract 3488: Truncated FGFR2 - a clinically actionable oncogene in multiple cancers
4. Data from Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms
5. Data from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
6. Data from RICTOR Amplification Defines a Novel Subset of Patients with Lung Cancer Who May Benefit from Treatment with mTORC1/2 Inhibitors
7. Supplementary Methods from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
8. Supplementary Table S3 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
9. 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
10. Supplementary Figure S2 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
11. Supplementary Methods, Figure Legends, Table Legend from EGFR Kinase Domain Duplication (EGFR-KDD) Is a Novel Oncogenic Driver in Lung Cancer That Is Clinically Responsive to Afatinib
12. Data from EGFR Fusions as Novel Therapeutic Targets in Lung Cancer
13. Supplementary Tables 1 through 3 and Supplementary Figures 1 through 4 from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade
14. Data from EGFR Kinase Domain Duplication (EGFR-KDD) Is a Novel Oncogenic Driver in Lung Cancer That Is Clinically Responsive to Afatinib
15. Supplementary Table S1A - S1B from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
16. Supplementary Figures S1 - S10 from EGFR Fusions as Novel Therapeutic Targets in Lung Cancer
17. Supplementary Methods, Figure Legends, Table Legends from EGFR Fusions as Novel Therapeutic Targets in Lung Cancer
18. Data from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
19. Supplementary Figures 1 - 6, Table 1 from EGFR Kinase Domain Duplication (EGFR-KDD) Is a Novel Oncogenic Driver in Lung Cancer That Is Clinically Responsive to Afatinib
20. Data from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade
21. 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
22. Supplementary Methods, Figures 1 - 5, Tables 1 - 5 from Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms
23. Supplementary Tables S1 - S3 from EGFR Fusions as Novel Therapeutic Targets in Lung Cancer
24. Figure S1, Figure S2, Table S1 from Anaplastic Lymphoma Kinase Mutation (ALK F1174C) in Small Cell Carcinoma of the Prostate and Molecular Response to Alectinib
25. Supplemental table 1 from Profiling of 149 Salivary Duct Carcinomas, Carcinoma Ex Pleomorphic Adenomas, and Adenocarcinomas, Not Otherwise Specified Reveals Actionable Genomic Alterations
26. Table S1 from Optimized EGFR Blockade Strategies in EGFR Addicted Gastroesophageal Adenocarcinomas
27. Supplemental Data from Individualized Molecular Analyses Guide Efforts (IMAGE): A Prospective Study of Molecular Profiling of Tissue and Blood in Metastatic Triple-Negative Breast Cancer
28. Supplemental methods from Profiling of 149 Salivary Duct Carcinomas, Carcinoma Ex Pleomorphic Adenomas, and Adenocarcinomas, Not Otherwise Specified Reveals Actionable Genomic Alterations
29. Supplemental Tables and Figures from Hybrid Capture–Based Genomic Profiling of Circulating Tumor DNA from Patients with Advanced Cancers of the Gastrointestinal Tract or Anus
30. Figure S3 from Optimized EGFR Blockade Strategies in EGFR Addicted Gastroesophageal Adenocarcinomas
31. Supplemental figure legend from Profiling of 149 Salivary Duct Carcinomas, Carcinoma Ex Pleomorphic Adenomas, and Adenocarcinomas, Not Otherwise Specified Reveals Actionable Genomic Alterations
32. Supplemental figure 1 from Profiling of 149 Salivary Duct Carcinomas, Carcinoma Ex Pleomorphic Adenomas, and Adenocarcinomas, Not Otherwise Specified Reveals Actionable Genomic Alterations
33. Supplementary Figure from The Genomics of Colorectal Cancer in Populations with African and European Ancestry
34. Data from The Genomics of Colorectal Cancer in Populations with African and European Ancestry
35. Supplementary Methods, Figures 1 - 5, Tables 1 - 5 from Diverse and Targetable Kinase Alterations Drive Histiocytic Neoplasms
36. Supplementary Methods, Figure Legends, Table Legends from EGFR Fusions as Novel Therapeutic Targets in Lung Cancer
37. Supplementary Table S3 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
38. Data from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade
39. 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
40. Supplementary Tables S1 - S3 from EGFR Fusions as Novel Therapeutic Targets in Lung Cancer
41. Supplementary Figure S3 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
42. Supplementary Methods from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
43. Supplementary Tables 1 through 3 and Supplementary Figures 1 through 4 from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade
44. Supplementary Figures S1 - S10 from EGFR Fusions as Novel Therapeutic Targets in Lung Cancer
45. Supplementary Figures 1 - 6, Table 1 from EGFR Kinase Domain Duplication (EGFR-KDD) Is a Novel Oncogenic Driver in Lung Cancer That Is Clinically Responsive to Afatinib
46. Supplementary Table S3 from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
47. Supplementary Methods, Figure Legends, Table Legend from EGFR Kinase Domain Duplication (EGFR-KDD) Is a Novel Oncogenic Driver in Lung Cancer That Is Clinically Responsive to Afatinib
48. Data from Activation of MET via Diverse Exon 14 Splicing Alterations Occurs in Multiple Tumor Types and Confers Clinical Sensitivity to MET Inhibitors
49. Supplementary Table S1A - S1B from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
50. Figure S4 from Optimized EGFR Blockade Strategies in EGFR Addicted Gastroesophageal Adenocarcinomas
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