1,286 results on '"Pao, William"'
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52. Supplementary Table 14 from A Meta-analysis of Somatic Mutations from Next Generation Sequencing of 241 Melanomas: A Road Map for the Study of Genes with Potential Clinical Relevance
53. Supplementary Table S2 from Dual Inhibition of EGFR with Afatinib and Cetuximab in Kinase Inhibitor–Resistant EGFR-Mutant Lung Cancer with and without T790M Mutations
54. Supplementary Figure 3 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
55. Supplementary Table 1 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
56. Supplementary Figure 9 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
57. Supplementary Methods from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
58. Supplementary Table S3 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
59. Supplementary Tables 1-2, 4, 7, 9, 10-11 from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
60. Supplementary Tables 3, 5, 6, 8 from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
61. Supplementary Figure S2 from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
62. Data from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
63. Supplementary Figure 2 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
64. Data from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
65. Supplementary Figure 1 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
66. Supplementary Figure 7 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
67. Supplementary Figures S1 through S4 from Optimizing the Sequence of Anti-EGFR–Targeted Therapy in EGFR-Mutant Lung Cancer
68. Supplementary Figure 4 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
69. Supplementary Table S1A - S1B from Comprehensive Genomic Profiling of Pancreatic Acinar Cell Carcinomas Identifies Recurrent RAF Fusions and Frequent Inactivation of DNA Repair Genes
70. Supplementary Materials and Methods from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
71. Supplementary Figures 1-11 from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
72. Supplementary Figure 5 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
73. Supplementary Figure 7 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
74. Supplementary Figure 6 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
75. Supplementary File 1 from A Meta-analysis of Somatic Mutations from Next Generation Sequencing of 241 Melanomas: A Road Map for the Study of Genes with Potential Clinical Relevance
76. Supplementary Figure 11 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
77. Supplementary Figures 1 through 16 from A Meta-analysis of Somatic Mutations from Next Generation Sequencing of 241 Melanomas: A Road Map for the Study of Genes with Potential Clinical Relevance
78. Supplementary Figure 3 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
79. Supplemental Figure Legends from Optimizing the Sequence of Anti-EGFR–Targeted Therapy in EGFR-Mutant Lung Cancer
80. Supplementary Figure 3 from HER2 Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in EGFR-Mutant Lung Cancers That Lack the Second-Site EGFRT790M Mutation
81. Supplementary Table 2 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
82. Supplementary Table 1 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
83. Supplementary Table 3 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
84. Supplementary Figure Legends 1-11 from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
85. Supplementary Methods from BRAFL597 Mutations in Melanoma Are Associated with Sensitivity to MEK Inhibitors
86. Supplementary Figure 4 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
87. Supplementary Figure Legends 1-5 from HER2 Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in EGFR-Mutant Lung Cancers That Lack the Second-Site EGFRT790M Mutation
88. Data from Optimizing the Sequence of Anti-EGFR–Targeted Therapy in EGFR-Mutant Lung Cancer
89. Supplementary Tables 1 through 13 and Supplementary Table 15 from A Meta-analysis of Somatic Mutations from Next Generation Sequencing of 241 Melanomas: A Road Map for the Study of Genes with Potential Clinical Relevance
90. Supplementary Figure 5 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
91. Supplementary Figure 6 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC
92. Supplementary Figure 1 from HER2 Amplification: A Potential Mechanism of Acquired Resistance to EGFR Inhibition in EGFR-Mutant Lung Cancers That Lack the Second-Site EGFRT790M Mutation
93. Supplementary Figure 2 from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
94. Data from AZD9291, an Irreversible EGFR TKI, Overcomes T790M-Mediated Resistance to EGFR Inhibitors in Lung Cancer
95. Supplementary Table 3 from Characteristics of Lung Cancers Harboring NRAS Mutations
96. Supplementary Figure 3 from Heterogeneous Mechanisms of Primary and Acquired Resistance to Third-Generation EGFR Inhibitors
97. CCR Translation for This Article from A Pilot Study of Volume Measurement as a Method of Tumor Response Evaluation to Aid Biomarker Development
98. Data from ALK Mutations Conferring Differential Resistance to Structurally Diverse ALK Inhibitors
99. Data from Analysis of Genetic Variants in Never-Smokers with Lung Cancer Facilitated by an Internet-Based Blood Collection Protocol: A Preliminary Report
100. Supplementary Figure 1 from FGFR1/3 Tyrosine Kinase Fusions Define a Unique Molecular Subtype of Non–Small Cell Lung Cancer
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