David W. Dawson
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View article: Antithrombin-binding heparan sulfate is ubiquitously expressed in epithelial cells and suppresses pancreatic tumorigenesis
Antithrombin-binding heparan sulfate is ubiquitously expressed in epithelial cells and suppresses pancreatic tumorigenesis Open
3-O-sulfation of heparan sulfate (HS) is the key determinant for binding and activation of antithrombin III (AT). This interaction is the basis of heparin treatment to prevent thrombotic events and excess coagulation. Antithrombin-binding …
View article: Self-amplifying NRF2–EZH2 epigenetic loop converts KRAS-initiated progenitors to invasive pancreatic cancer
Self-amplifying NRF2–EZH2 epigenetic loop converts KRAS-initiated progenitors to invasive pancreatic cancer Open
View article: Emerin is an effector of oncogenic KRAS-driven nuclear dynamics in pancreatic cancer
Emerin is an effector of oncogenic KRAS-driven nuclear dynamics in pancreatic cancer Open
For over a century, scientists reported the disruption of normal nuclear shape and size in cancer. These changes have long been used as tools for diagnosis and staging of malignancies. However, to date, the mechanisms underlying these aber…
View article: Colorectal Cancer Arising in a Colon Interposition After Esophageal Reconstruction: The Medical Oncology Perspective
Colorectal Cancer Arising in a Colon Interposition After Esophageal Reconstruction: The Medical Oncology Perspective Open
Severe esophageal disease can be remedied with colonic interposition, a surgical procedure in which the resected esophagus is replaced by a segment of colon. The development of adenocarcinoma in the colon conduit is a rare but growing long…
View article: nSMase2-mediated exosome secretion shapes the tumor microenvironment to immunologically support pancreatic cancer
nSMase2-mediated exosome secretion shapes the tumor microenvironment to immunologically support pancreatic cancer Open
The pleiotropic roles of nSMase2-generated ceramide include regulation of intracellular ceramide signaling and exosome biogenesis. We investigated the effects of eliminating nSMase2 on early and advanced PDA, including its influence on the…
View article: Oncogenic pathway signatures predict the risk of progression and recurrence in well‐differentiated pancreatic neuroendocrine tumors
Oncogenic pathway signatures predict the risk of progression and recurrence in well‐differentiated pancreatic neuroendocrine tumors Open
Background Pancreatic neuroendocrine tumors (pNETs) are genomically diverse tumors. The management of newly diagnosed well‐differentiated pNETs is limited by a lack of sensitivity of existing biomarkers for prognostication. Our goal was to…
View article: Freehand Resection of a Stoma Polyp Using Endoscopic-Based Techniques
Freehand Resection of a Stoma Polyp Using Endoscopic-Based Techniques Open
CASE REPORT Colon polyps originating at stoma sites are a rare entity. In this report, we describe a unique case of an adenomatous stoma polyp that was resected without sedation using simplified endoscopic-based techniques. Informed consen…
View article: Cell polarity proteins promote macropinocytosis in response to metabolic stress
Cell polarity proteins promote macropinocytosis in response to metabolic stress Open
Macropinocytosis has emerged as a nutrient-scavenging pathway that cancer cells exploit to survive the nutrient-deprived conditions of the tumor microenvironment. Cancer cells are especially reliant on glutamine for their survival, and in …
View article: Promoter Methylation Leads to Hepatocyte Nuclear Factor 4A Loss and Pancreatic Cancer Aggressiveness
Promoter Methylation Leads to Hepatocyte Nuclear Factor 4A Loss and Pancreatic Cancer Aggressiveness Open
View article: Data from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Data from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Cancer-associated fibroblast (CAF) heterogeneity is increasingly appreciated, but the origins and functions of distinct CAF subtypes remain poorly understood. The abundant and transcriptionally diverse CAF population in pancreatic ductal a…
View article: Table S2 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Table S2 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Table S2
View article: Table S1 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Table S1 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Table S1
View article: Supplementary Methods from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Supplementary Methods from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Supplementary Methods
View article: Supplementary Methods from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Supplementary Methods from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Supplementary Methods
View article: Table S2 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Table S2 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Table S2
View article: Data from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Data from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Cancer-associated fibroblast (CAF) heterogeneity is increasingly appreciated, but the origins and functions of distinct CAF subtypes remain poorly understood. The abundant and transcriptionally diverse CAF population in pancreatic ductal a…
View article: Supplementary Figures from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Supplementary Figures from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Figures S1-S3
View article: Supplementary Figures from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Supplementary Figures from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Figures S1-S3
View article: Table S1 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts
Table S1 from Mesenchymal Lineage Heterogeneity Underlies Nonredundant Functions of Pancreatic Cancer–Associated Fibroblasts Open
Table S1
View article: Supplementary Figure from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer
Supplementary Figure from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer Open
Supplementary Figure from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer
View article: Supplementary Data from Chemotherapy-Induced Inflammatory Gene Signature and Protumorigenic Phenotype in Pancreatic CAFs via Stress-Associated MAPK
Supplementary Data from Chemotherapy-Induced Inflammatory Gene Signature and Protumorigenic Phenotype in Pancreatic CAFs via Stress-Associated MAPK Open
Figures S1-4 and Table S1 Figure S1. N-CAFs and R-CAFs were exposed to the indicated concentrations of gemcitabine for 72h, and viability was measured via MTT assay. 3 biologic replicates were included in the experiment. **p{less than or e…
View article: Data Supplement from The CREB-Binding Protein Inhibitor ICG-001 Suppresses Pancreatic Cancer Growth
Data Supplement from The CREB-Binding Protein Inhibitor ICG-001 Suppresses Pancreatic Cancer Growth Open
Supplemental Table 1. PCR primers.
View article: Supplementary Figure S2 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Supplementary Figure S2 from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Supplementary Figure S2 shows analysis for macrophages in cytokeratin-19 positive regions of ADM (A), and analysis for ICAM-1, macrophages and cytokeratin-19 in PanIN lesions (B).
View article: Data Supplement from The CREB-Binding Protein Inhibitor ICG-001 Suppresses Pancreatic Cancer Growth
Data Supplement from The CREB-Binding Protein Inhibitor ICG-001 Suppresses Pancreatic Cancer Growth Open
Supplemental Figure 4. Gene ontology terms enriched in gene expression microarray analysis following ICG-001 treatment.
View article: Data from Calcipotriol Targets LRP6 to Inhibit Wnt Signaling in Pancreatic Cancer
Data from Calcipotriol Targets LRP6 to Inhibit Wnt Signaling in Pancreatic Cancer Open
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy in need of more effective treatment approaches. One potential therapeutic target is Wnt/β-catenin signaling, which plays important roles in PDAC tumor initiation and progr…
View article: Data Supplement from The CREB-Binding Protein Inhibitor ICG-001 Suppresses Pancreatic Cancer Growth
Data Supplement from The CREB-Binding Protein Inhibitor ICG-001 Suppresses Pancreatic Cancer Growth Open
Supplemental Figure 2. H&E images of tumors and normal organs from orthotopic xenograft assay with ICG-001.
View article: Supplementary Table from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer
Supplementary Table from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer Open
Supplementary Table from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer
View article: Data from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer
Data from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer Open
WNT signaling promotes pancreatic ductal adenocarcinoma (PDAC) through diverse effects on proliferation, differentiation, survival, and stemness. A subset of PDAC with inactivating mutations in ring finger protein 43 (RNF43) show gr…
View article: Data from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions
Data from Mutant KRAS–Induced Expression of ICAM-1 in Pancreatic Acinar Cells Causes Attraction of Macrophages to Expedite the Formation of Precancerous Lesions Open
Desmoplasia and an inflammatory environment are defining features of pancreatic cancer. Unclear is how pancreatic cells that undergo oncogenic transformation can cross-talk with immune cells and how this contributes to the development of p…
View article: Data from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer
Data from Porcupine Inhibition Disrupts Mitochondrial Function and Homeostasis in WNT Ligand–Addicted Pancreatic Cancer Open
WNT signaling promotes pancreatic ductal adenocarcinoma (PDAC) through diverse effects on proliferation, differentiation, survival, and stemness. A subset of PDAC with inactivating mutations in ring finger protein 43 (RNF43) show gr…