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101. Data from Genetic Events That Limit the Efficacy of MEK and RTK Inhibitor Therapies in a Mouse Model of KRAS-Driven Pancreatic Cancer

102. Data from A Genome-Wide Screen Reveals Functional Gene Clusters in the Cancer Genome and Identifies EphA2 as a Mitogen in Glioblastoma

103. Data from Common and Distinct Genomic Events in Sporadic Colorectal Cancer and Diverse Cancer Types

104. Supplementary Table 1 from Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

106. Supplementary Table 2 from Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

110. Supplementary Table 1 from Up-Regulation of c-Jun Inhibits Proliferation and Induces Apoptosis via Caspase-Triggered c-Abl Cleavage in Human Multiple Myeloma

111. Supplementary Table 4 from Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

114. Supplementary Figures 1-4 from Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

116. Supplementary Legends and Figures 1-2 from Up-Regulation of c-Jun Inhibits Proliferation and Induces Apoptosis via Caspase-Triggered c-Abl Cleavage in Human Multiple Myeloma

117. Supplementary Methods from Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

118. supplementary material and method from Genetic Events That Limit the Efficacy of MEK and RTK Inhibitor Therapies in a Mouse Model of KRAS-Driven Pancreatic Cancer

119. Supplementary Table 3 from Marked Genomic Differences Characterize Primary and Secondary Glioblastoma Subtypes and Identify Two Distinct Molecular and Clinical Secondary Glioblastoma Entities

120. Supplementary Methods and Materials from Common and Distinct Genomic Events in Sporadic Colorectal Cancer and Diverse Cancer Types

122. Supplementary Figures 1-4 from Direct Transcriptional Activation of Promyelocytic Leukemia Protein by IFN Regulatory Factor 3 Induces the p53-Dependent Growth Inhibition of Cancer Cells

125. Supplementary Table 2 from Common and Distinct Genomic Events in Sporadic Colorectal Cancer and Diverse Cancer Types

126. Supplementary Table 1 from A Genome-Wide Screen Reveals Functional Gene Clusters in the Cancer Genome and Identifies EphA2 as a Mitogen in Glioblastoma

127. Data from Direct Transcriptional Activation of Promyelocytic Leukemia Protein by IFN Regulatory Factor 3 Induces the p53-Dependent Growth Inhibition of Cancer Cells

129. supplementary Figures S1-S10 from Genetic Events That Limit the Efficacy of MEK and RTK Inhibitor Therapies in a Mouse Model of KRAS-Driven Pancreatic Cancer

131. Supplementary Table 2 from A Genome-Wide Screen Reveals Functional Gene Clusters in the Cancer Genome and Identifies EphA2 as a Mitogen in Glioblastoma

133. Supplementary Figures 1-5 from A Genome-Wide Screen Reveals Functional Gene Clusters in the Cancer Genome and Identifies EphA2 as a Mitogen in Glioblastoma

135. Supplementary Figure 2 from Common and Distinct Genomic Events in Sporadic Colorectal Cancer and Diverse Cancer Types

136. Supplementary Information from A Genome-Wide Screen Reveals Functional Gene Clusters in the Cancer Genome and Identifies EphA2 as a Mitogen in Glioblastoma

138. Author Correction: An enolase inhibitor for the targeted treatment of ENO1-deleted cancers

139. Effective combinatorial immunotherapy for castration-resistant prostate cancer

140. Targeting T cell checkpoints 41BB and LAG3 and myeloid cell CXCR1/CXCR2 results in antitumor immunity and durable response in pancreatic cancer

142. Abstract PR011: Histone demethylase KDM5D drives sex-specific differences in colorectal cancer

143. Abstract IA014: Synthetic essentiality identifies TDO2 as a key target in APC-deficient CRC

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