Evan S. Ong
Evan S. Ong has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Colin J. Rog
Division of Surgical Oncology, Department of Surgery, Swedish Medical Center, Seattle, Washington
2 shared publications - Mohamed Alassas
Department of Surgery, Division of Surgical Oncology, Swedish Medical Center, 747 Broadway, Heath 10, Suite 1003, Seattle, WA, 98122, USA
2 shared publications - Shelby Reiter
Department of Surgery, Division of Surgical Oncology, Swedish Medical Center, 747 Broadway, Heath 10, Suite 1003, Seattle, WA, 98122, USA
2 shared publications - Adam J. Bograd
Division of Thoracic Surgery and Interventional Pulmonology, Swedish Cancer Institute, Seattle, WA
1 shared publication - Alex Cardenas
Western Surgical Group
1 shared publication - Brenna A. Rheinheimer
University of Arizona
1 shared publication
Latest Publications
- 31 May 2025
- Published by Springer Nature
- p. 75-79
Hypoglycemia Secondary to Anti-PD-1 Therapy
- 1 June 2022
- Published by Elsevier in The American Journal of Surgery
- Vol. 223 (6) , 1183-1186
Progression to pseudomyxoma peritonei in patients with low grade appendiceal mucinous neoplasms discovered at time of appendectomy
- 1 June 2022
- Published by Elsevier in The American Journal of Surgery
- Vol. 223 (6) , 1183-1186
Progression to pseudomyxoma peritonei in patients with low grade appendiceal mucinous neoplasms discovered at time of appendectomy
- 18 March 2021
- Published by Elsevier in The American Journal of Surgery
- Vol. 221 (6) , 1200-1202
Optimal oncologic and perioperative outcomes of cytoreductive surgery with hyperthermic intraperitoneal chemotherapy are attainable at a community center
- 18 March 2021
- Published by Elsevier in The American Journal of Surgery
- Vol. 221 (6) , 1200-1202
Optimal oncologic and perioperative outcomes of cytoreductive surgery with hyperthermic intraperitoneal chemotherapy are attainable at a community center
- Open Access
Inhibition of Sphingosine-1-Phosphate signaling in pancreatic ductal adenocarcinoma leads to downregulation of growth and invasion
Background: Deregulated phosphorylation of sphingosine by the sphingosine kinases and signaling through the EDG family of receptors enhances growth and survival in many cell types. Therefore, we sought to elucidate the effect of alterations in the ceramide/sphingosine/S1P rheostat on driving human pancreatic ductal adenocarcinoma towards a malignant phenotype. Methods: Pancreatic cancer cell lines were treated with exogenous S1P, FTY720, and siRNA to Sphk1. Migration was evaluated by wound healing assays, cell growth by MTT assays, and invasion by tumorsphere assays. Expression of S1PR1, S1PR3, Sphk1, and Sphk2 were measured by quantitative PCR, western blot, and immunohistochemistry. Results: S1PR1, S1PR3, and Sphk2 were overexpressed in all pancreatic cancer cell lines. Sphk1 translocated from the cytoplasm to the nucleus in cells located at the leading edge of cell clusters. Exogenous S1P increased cell migration while treatment with FTY720 and Sphk1 siRNA decreased cell growth and invasion. Conclusions: Our results suggest that increased S1PR1 expression may be an early event in pancreatic cancer pathogenesis. Additionally, altered Sphk1 localization may provide a mechanism through which pancreatic ductal adenocarcinoma cells at the leading edge invade into the surrounding matrix. Finally, inhibition of sphingosine-1-phosphate signaling may provide a novel therapeutic target for patients with metastatic disease.
Open AccessInhibition of Sphingosine-1-Phosphate signaling in pancreatic ductal adenocarcinoma leads to downregulation of growth and invasion
Background: Deregulated phosphorylation of sphingosine by the sphingosine kinases and signaling through the EDG family of receptors enhances growth and survival in many cell types. Therefore, we sought to elucidate the effect of alterations in the ceramide/sphingosine/S1P rheostat on driving human pancreatic ductal adenocarcinoma towards a malignant phenotype. Methods: Pancreatic cancer cell lines were treated with exogenous S1P, FTY720, and siRNA to Sphk1. Migration was evaluated by wound healing assays, cell growth by MTT assays, and invasion by tumorsphere assays. Expression of S1PR1, S1PR3, Sphk1, and Sphk2 were measured by quantitative PCR, western blot, and immunohistochemistry. Results: S1PR1, S1PR3, and Sphk2 were overexpressed in all pancreatic cancer cell lines. Sphk1 translocated from the cytoplasm to the nucleus in cells located at the leading edge of cell clusters. Exogenous S1P increased cell migration while treatment with FTY720 and Sphk1 siRNA decreased cell growth and invasion. Conclusions: Our results suggest that increased S1PR1 expression may be an early event in pancreatic cancer pathogenesis. Additionally, altered Sphk1 localization may provide a mechanism through which pancreatic ductal adenocarcinoma cells at the leading edge invade into the surrounding matrix. Finally, inhibition of sphingosine-1-phosphate signaling may provide a novel therapeutic target for patients with metastatic disease.