705 results on '"Frederick, Dennie T"'
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52. Data from ER Translocation of the MAPK Pathway Drives Therapy Resistance in BRAF-Mutant Melanoma
53. Supplementary Methods, Figure Legends from Reduced Proteolytic Shedding of Receptor Tyrosine Kinases Is a Post-Translational Mechanism of Kinase Inhibitor Resistance
54. Supplementary Figure S3 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
55. Supplementary Table S1 from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
56. Data from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
57. Supplementary Figure S6 from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
58. Supplementary Table 3 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
59. Data from The Immune Microenvironment Confers Resistance to MAPK Pathway Inhibitors through Macrophage-Derived TNFα
60. Supplementary Table 2 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
61. Data from Reduced Proteolytic Shedding of Receptor Tyrosine Kinases Is a Post-Translational Mechanism of Kinase Inhibitor Resistance
62. Data from SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
63. Supplementary Movie 2 (SM2) from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
64. Supplementary Figures from ER Translocation of the MAPK Pathway Drives Therapy Resistance in BRAF-Mutant Melanoma
65. Supplementary Figure Legends from EPHA2 Is a Mediator of Vemurafenib Resistance and a Novel Therapeutic Target in Melanoma
66. Supplementary Materials and Methods from A Melanoma Cell State Distinction Influences Sensitivity to MAPK Pathway Inhibitors
67. Supplementary Movie 1 from SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
68. Supplementary Figure Legend from Elucidating Distinct Roles for NF1 in Melanomagenesis
69. Supplementary Figures S1 - S9, Table S1 from The Immune Microenvironment Confers Resistance to MAPK Pathway Inhibitors through Macrophage-Derived TNFα
70. Data from Elucidating Distinct Roles for NF1 in Melanomagenesis
71. Supplementary Table 2 from SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
72. Supplementary Table 4 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
73. Supplementary Table 1 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
74. Supplementary Tables 1 through 3 and Supplementary Figures 1 through 4 from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade
75. Supplementary Table 6 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
76. Supplementary Movie 1 (SM1) from Changes in Aged Fibroblast Lipid Metabolism Induce Age-Dependent Melanoma Cell Resistance to Targeted Therapy via the Fatty Acid Transporter FATP2
77. Supplementary Movie 2 from SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
78. Data from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
79. Supplementary Figures from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
80. Supplementary Figure 1 from Elucidating Distinct Roles for NF1 in Melanomagenesis
81. Supplementary Figures S1-S19 from A Melanoma Cell State Distinction Influences Sensitivity to MAPK Pathway Inhibitors
82. Data from A Melanoma Cell State Distinction Influences Sensitivity to MAPK Pathway Inhibitors
83. Supplementary Movie 1 from ER Translocation of the MAPK Pathway Drives Therapy Resistance in BRAF-Mutant Melanoma
84. Supplementary Data Figure Legends from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
85. Data from Targeted Next Generation Sequencing Identifies Markers of Response to PD-1 Blockade
86. Data from Response to BRAF Inhibition in Melanoma Is Enhanced When Combined with Immune Checkpoint Blockade
87. Supplementary Movie 2 from ER Translocation of the MAPK Pathway Drives Therapy Resistance in BRAF-Mutant Melanoma
88. Supplementary Table 3 from SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
89. Supplementary Table 1 from SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
90. Data Supplement from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
91. Supplementary tables from ER Translocation of the MAPK Pathway Drives Therapy Resistance in BRAF-Mutant Melanoma
92. Supplementary Table 5 from MAP Kinase Pathway Alterations in BRAF-Mutant Melanoma Patients with Acquired Resistance to Combined RAF/MEK Inhibition
93. Supplementary Table 2 from Hypoxia Induces Phenotypic Plasticity and Therapy Resistance in Melanoma via the Tyrosine Kinase Receptors ROR1 and ROR2
94. Supplementary Tables S1-S2 from A Melanoma Cell State Distinction Influences Sensitivity to MAPK Pathway Inhibitors
95. Supplementary Figure Legend from Response to BRAF Inhibition in Melanoma Is Enhanced When Combined with Immune Checkpoint Blockade
96. Supplementary Data from SPANX Control of Lamin A/C Modulates Nuclear Architecture and Promotes Melanoma Growth
97. Supplementary Figures from Response to BRAF Inhibition in Melanoma Is Enhanced When Combined with Immune Checkpoint Blockade
98. Data from Neural Crest-Like Stem Cell Transcriptome Analysis Identifies LPAR1 in Melanoma Progression and Therapy Resistance
99. Table S5 from Neural Crest-Like Stem Cell Transcriptome Analysis Identifies LPAR1 in Melanoma Progression and Therapy Resistance
100. Supplementary Figures from Neural Crest-Like Stem Cell Transcriptome Analysis Identifies LPAR1 in Melanoma Progression and Therapy Resistance
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