Brian J. Long
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View article: Patient-derived colorectal microtumors predict response to anti-PD-1 therapy
Patient-derived colorectal microtumors predict response to anti-PD-1 therapy Open
Immune checkpoint inhibitors have made remarkable impacts in treating various cancers, including colorectal cancer (CRC). However, CRC still remains a leading cause of cancer-related deaths. While microsatellite instability (MSI) CRC has s…
Data from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Many tumor types harbor alterations in the Hippo pathway, including mesothelioma, where a high percentage of cases are considered YAP1/TEAD dependent. Identification of autopalmitoylation sites in the hydrophobic palmitate pocket of TEADs,…
Figure S3 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Pathway analysis after MRK-A treatment in vitro and in vivo characterization.
Supplementary table 1 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Supplementary table 1
Figure S3 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Pathway analysis after MRK-A treatment in vitro and in vivo characterization.
Figure S2 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
In vitro RNA-Seq characterization of MRK-A.
Figure S2 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
In vitro RNA-Seq characterization of MRK-A.
Figure S4 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
MRK-A combination with immune checkpoint blockade.
Figure S4 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
MRK-A combination with immune checkpoint blockade.
Figure S1 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
In vitro characterization of MRK-A.
Supplementary Methods from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Supplementary/extended materials and methods
Figure S5 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
In vivo pathway analysis after MRK-A treatment.
Figure S6 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Characterization of HGF impact on MRK-A activity.
Supplementary table 2 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Supplementary table 2
Supplementary table 2 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Supplementary table 2
Figure S5 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
In vivo pathway analysis after MRK-A treatment.
Figure S6 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Characterization of HGF impact on MRK-A activity.
Data from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Many tumor types harbor alterations in the Hippo pathway, including mesothelioma, where a high percentage of cases are considered YAP1/TEAD dependent. Identification of autopalmitoylation sites in the hydrophobic palmitate pocket of TEADs,…
Supplementary Methods from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Supplementary/extended materials and methods
Figure S1 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
In vitro characterization of MRK-A.
Supplementary table 1 from Activation of Hepatocyte Growth Factor/MET Signaling as a Mechanism of Acquired Resistance to a Novel YAP1/TEAD Small Molecule Inhibitor Open
Supplementary table 1
View article: Figure S2 from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors
Figure S2 from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors Open
Supplemental Figure 2: STING agonists stimulate cytokines in tumor, plasma and peripheral tissues following IT dosing.
View article: Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models
Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models Open
Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models
View article: Figure S1 from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors
Figure S1 from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors Open
Supplemental Figure 1: Day 10 tumor volume of injected (InjT) and noninjected (Non-injT) tumors following intratumoral (IT) injection with MSA-1
View article: Supplementary Data from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors
Supplementary Data from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors Open
Supplementary Methods and Figures
View article: Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models
Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models Open
Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models
Data from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors Open
The innate immune agonist STING (STimulator of INterferon Genes) binds its natural ligand 2′3′-cGAMP (cyclic guanosine-adenosine monophosphate) and initiates type I IFN production. This promotes systemic antigen-specific CD8+ T-cell primin…
View article: Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models
Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models Open
Supplementary Data from Reverse Translating Molecular Determinants of Anti–Programmed Death 1 Immunotherapy Response in Mouse Syngeneic Tumor Models
Figure S2 from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors Open
Supplemental Figure 2: STING agonists stimulate cytokines in tumor, plasma and peripheral tissues following IT dosing.
Table S1 from STimulator of INterferon Genes Agonism Accelerates Antitumor Activity in Poorly Immunogenic Tumors Open
Supplemental Table 1: Log2Ratio and p values for all 310 genes shown in Figure 6