1,260 results on '"Schwartz, Gary K."'
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102. Supplementary Figure 5 from Identification of Unique MEK-Dependent Genes in GNAQ Mutant Uveal Melanoma Involved in Cell Growth, Tumor Cell Invasion, and MEK Resistance
103. Supplementary Data from Randomized Phase II Trial and Tumor Mutational Spectrum Analysis from Cabozantinib versus Chemotherapy in Metastatic Uveal Melanoma (Alliance A091201)
104. Supplementary Figure 3 from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
105. Supplementary Table S1 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
106. Supplementary Figure 7 from Identification of Unique MEK-Dependent Genes in GNAQ Mutant Uveal Melanoma Involved in Cell Growth, Tumor Cell Invasion, and MEK Resistance
107. Data from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
108. Supplementary Figure S1 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
109. Supplementary Figure 2 from Phase I, Dose-Escalation Trial of the Oral Cyclin-Dependent Kinase 4/6 Inhibitor PD 0332991, Administered Using a 21-Day Schedule in Patients with Advanced Cancer
110. Supplementary Data 3 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
111. Supplementary Materials and Methods, Figure Legends from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
112. Supplementary Data from A Phase Ib/II Randomized Study of RO4929097, a Gamma-Secretase or Notch Inhibitor with or without Vismodegib, a Hedgehog Inhibitor, in Advanced Sarcoma
113. Supplementary Figure 1 from Identification of Unique MEK-Dependent Genes in GNAQ Mutant Uveal Melanoma Involved in Cell Growth, Tumor Cell Invasion, and MEK Resistance
114. Supplementary Data 4 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
115. Supplementary Figure Legend from Phase II Trial of MEK Inhibitor Selumetinib (AZD6244, ARRY-142886) in Patients with BRAFV600E/K-Mutated Melanoma
116. Supplementary Data 2 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
117. Supplementary Data 5 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
118. Supplementary Figure 6 from Identification of Unique MEK-Dependent Genes in GNAQ Mutant Uveal Melanoma Involved in Cell Growth, Tumor Cell Invasion, and MEK Resistance
119. Data from A Phase Ib/II Randomized Study of RO4929097, a Gamma-Secretase or Notch Inhibitor with or without Vismodegib, a Hedgehog Inhibitor, in Advanced Sarcoma
120. Supplementary Figure 6 from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
121. Supplementary Figure 1 from Phase I, Dose-Escalation Trial of the Oral Cyclin-Dependent Kinase 4/6 Inhibitor PD 0332991, Administered Using a 21-Day Schedule in Patients with Advanced Cancer
122. Supplementary Figure 1B from Phase II Trial of MEK Inhibitor Selumetinib (AZD6244, ARRY-142886) in Patients with BRAFV600E/K-Mutated Melanoma
123. Supplementary Figure 4 from Identification of Unique MEK-Dependent Genes in GNAQ Mutant Uveal Melanoma Involved in Cell Growth, Tumor Cell Invasion, and MEK Resistance
124. Supplementary Table from AZD7762, a novel checkpoint kinase inhibitor, drives checkpoint abrogation and potentiates DNA-targeted therapies
125. Supplementary Figure 5 from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
126. Supplementary Figure Legends 1-2 from Phase I, Dose-Escalation Trial of the Oral Cyclin-Dependent Kinase 4/6 Inhibitor PD 0332991, Administered Using a 21-Day Schedule in Patients with Advanced Cancer
127. Supplementary Data 6 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
128. Supplementary Data from Imaging Colon Cancer Response Following Treatment with AZD1152: A Preclinical Analysis of [18F]Fluoro-2-deoxyglucose and 3′-deoxy-3′-[18F]Fluorothymidine Imaging
129. Supplementary Figure 8 from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
130. Supplementary Figure S1 from The Topoisomerase I Poison CPT-11 Enhances the Effect of the Aurora B Kinase Inhibitor AZD1152 both In vitro and In vivo
131. Supplementary Figure 3 from Phase II Trial of MEK Inhibitor Selumetinib (AZD6244, ARRY-142886) in Patients with BRAFV600E/K-Mutated Melanoma
132. Supplementary Figure 7 from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
133. Supplementary Data 7 from Inhibition of NF-κB–Dependent Signaling Enhances Sensitivity and Overcomes Resistance to BET Inhibition in Uveal Melanoma
134. Supplementary Figure 3 from Identification of Unique MEK-Dependent Genes in GNAQ Mutant Uveal Melanoma Involved in Cell Growth, Tumor Cell Invasion, and MEK Resistance
135. Supplementary Figure 2 from Identification of Unique MEK-Dependent Genes in GNAQ Mutant Uveal Melanoma Involved in Cell Growth, Tumor Cell Invasion, and MEK Resistance
136. Supplementary Figure 4 from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
137. Supplementary Material 2 from CHIR-124, a Novel Potent Inhibitor of Chk1, Potentiates the Cytotoxicity of Topoisomerase I Poisons In vitro and In vivo
138. Supplementary Figures 1 - 2 from Sustained Inhibition of Receptor Tyrosine Kinases and Macrophage Depletion by PLX3397 and Rapamycin as a Potential New Approach for the Treatment of MPNSTs
139. Supplementary Table 1 from The Cyclin-Dependent Kinase Inhibitor Flavopiridol Potentiates Doxorubicin Efficacy in Advanced Sarcomas: Preclinical Investigations and Results of a Phase I Dose-Escalation Clinical Trial
140. Supplementary Movie 1 from Potentiation of Cytotoxicity of Topoisomerase I Poison by Concurrent and Sequential Treatment with the Checkpoint Inhibitor UCN-01 Involves Disparate Mechanisms Resulting in Either p53-Independent Clonogenic Suppression or p53-Dependent Mitotic Catastrophe
141. Supplementary Figure 1 from Differentiation-Related Gene-1 Decreases Bim Stability by Proteasome-Mediated Degradation
142. Supplementary Figure Legends 1-2, Methods from Differentiation-Related Gene-1 Decreases Bim Stability by Proteasome-Mediated Degradation
143. Data from Differentiation-Related Gene-1 Decreases Bim Stability by Proteasome-Mediated Degradation
144. Supplementary Movie 3 from Potentiation of Cytotoxicity of Topoisomerase I Poison by Concurrent and Sequential Treatment with the Checkpoint Inhibitor UCN-01 Involves Disparate Mechanisms Resulting in Either p53-Independent Clonogenic Suppression or p53-Dependent Mitotic Catastrophe
145. Data from PDGF Receptor Alpha Is an Alternative Mediator of Rapamycin-Induced Akt Activation: Implications for Combination Targeted Therapy of Synovial Sarcoma
146. Data from γ-Secretase Inhibitors Abrogate Oxaliplatin-Induced Activation of the Notch-1 Signaling Pathway in Colon Cancer Cells Resulting in Enhanced Chemosensitivity
147. Supplementary Figures 1-2, Tables 1-4 from Gene Expression Profiling of Liposarcoma Identifies Distinct Biological Types/Subtypes and Potential Therapeutic Targets in Well-Differentiated and Dedifferentiated Liposarcoma
148. Supplementary Movie 2 from Potentiation of Cytotoxicity of Topoisomerase I Poison by Concurrent and Sequential Treatment with the Checkpoint Inhibitor UCN-01 Involves Disparate Mechanisms Resulting in Either p53-Independent Clonogenic Suppression or p53-Dependent Mitotic Catastrophe
149. Supplementary Figure 2 from γ-Secretase Inhibitors Abrogate Oxaliplatin-Induced Activation of the Notch-1 Signaling Pathway in Colon Cancer Cells Resulting in Enhanced Chemosensitivity
150. Supplementary Figure 1 from PDGF Receptor Alpha Is an Alternative Mediator of Rapamycin-Induced Akt Activation: Implications for Combination Targeted Therapy of Synovial Sarcoma
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