Search

Your search keyword '"Pao, William"' showing total 1,286 results

Search Constraints

Start Over You searched for: Author "Pao, William" Remove constraint Author: "Pao, William"
1,286 results on '"Pao, William"'

Search Results

51. Supplementary Figure 8 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC

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

76. Supplementary Figure 11 from Discovery of a Mutant-Selective Covalent Inhibitor of EGFR that Overcomes T790M-Mediated Resistance in NSCLC

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

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

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

Catalog

Books, media, physical & digital resources