Yogev Sela
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View article: Hypermetabolic state is associated with circadian rhythm disruption in mouse and human cancer cells
Hypermetabolic state is associated with circadian rhythm disruption in mouse and human cancer cells Open
Crosstalk between metabolism and circadian rhythms is a fundamental building block of multicellular life, and disruption of this reciprocal communication could be relevant to disease. Here, we investigated whether maintenance of circadian …
View article: Hypermetabolic state is associated with circadian rhythm disruption in mouse and human cancer cells
Hypermetabolic state is associated with circadian rhythm disruption in mouse and human cancer cells Open
Crosstalk between cellular metabolism and circadian rhythms is a fundamental building block of multicellular life, and disruption of this reciprocal communication could be relevant to degenerative disease, including cancer. Here, we invest…
Intratumoral Administration of High-Concentration Nitric Oxide and Anti-mPD-1 Treatment Improves Tumor Regression Rates and Survival in CT26 Tumor-Bearing Mice Open
Background: Immune checkpoint inhibitors have transformed clinical oncology. However, their use is limited as response is observed in only ~20–50% of patients. Previously, we demonstrated that treating CT26 tumor-bearing mice with ultra-hi…
P14.09.B IS BLOOD-DERIVED EXOSOMAL HTERT TRANSCRIPT A MARKER OF ONCOGENIC ACTIVITY IN PRIMARY BRAIN TUMORS? AN EXPLORATORY STUDY Open
BACKGROUND In order to proliferate indefinitely, all tumors require a telomere maintenance mechanism. The expression of human telomerase reverse transcriptase (hTERT) enables telomere maintenance and provides cancer cells with limitless re…
Supplementary Data from Acetyl-CoA Metabolism Supports Multistep Pancreatic Tumorigenesis Open
Figures S1-S7 and Table S1
Data from Acetyl-CoA Metabolism Supports Multistep Pancreatic Tumorigenesis Open
Pancreatic ductal adenocarcinoma (PDA) has a poor prognosis, and new strategies for prevention and treatment are urgently needed. We previously reported that histone H4 acetylation is elevated in pancreatic acinar cells harboring Kras muta…
View article: Data from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i>
Data from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i> Open
Activation of Wnt signaling is among the earliest events in colon cancer development. It is achieved either via activating mutations in the CTNNB1 gene encoding β-catenin, the key transcription factor in the Wnt pathway, or most commonly b…
Supplementary Data from Acetyl-CoA Metabolism Supports Multistep Pancreatic Tumorigenesis Open
Figures S1-S7 and Table S1
View article: Supplementary Figures 1 and 2 from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i>
Supplementary Figures 1 and 2 from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i> Open
S1. DKK3 and Wnt signaling in CRC cells. S2. Derivation of murine colorectal tumoroids.
View article: Data from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i>
Data from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i> Open
Activation of Wnt signaling is among the earliest events in colon cancer development. It is achieved either via activating mutations in the CTNNB1 gene encoding β-catenin, the key transcription factor in the Wnt pathway, or most commonly b…
View article: Supplementary Figures 1 and 2 from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i>
Supplementary Figures 1 and 2 from MYC Hyperactivates Wnt Signaling in <i>APC</i>/<i>CTNNB1</i>-Mutated Colorectal Cancer Cells through miR-92a–Dependent Repression of <i>DKK3</i> Open
S1. DKK3 and Wnt signaling in CRC cells. S2. Derivation of murine colorectal tumoroids.
Data from Acetyl-CoA Metabolism Supports Multistep Pancreatic Tumorigenesis Open
Pancreatic ductal adenocarcinoma (PDA) has a poor prognosis, and new strategies for prevention and treatment are urgently needed. We previously reported that histone H4 acetylation is elevated in pancreatic acinar cells harboring Kras muta…
View article: Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Solid tumors possess heterogeneous metabolic microenvironments where oxygen and nutrient availability are plentiful (fertile regions) or scarce (arid regions). While cancer cells residing in fertile regions proliferate rapidly, most cancer…
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Figure from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Figure from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Solid tumors possess heterogeneous metabolic microenvironments where oxygen and nutrient availability are plentiful (fertile regions) or scarce (arid regions). While cancer cells residing in fertile regions proliferate rapidly, most cancer…
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Table from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer Open
Supplementary Data from Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer