Persistent Link:
http://hdl.handle.net/10150/306974
Title:
Sphingosine-1-Phosphate in Pancreatic Ductal Adenocarcinoma
Author:
Cardenas, Alex
Issue Date:
2013
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
Pancreatic ductal adenocarcinoma is an extremely lethal cancer that is difficult to treat. A better understanding of the biology of pancreatic ductal cancer will help to develop targeted therapies that may improve clinical outcomes. Recently, the lipid signaling molecule sphingosine-1-phosphate (S1P) has emerged as a driver of malignant behavior in many types of cancer. Its role in pancreatic cancer remains unknown. Pancreatic cancer cells express high levels of the S1P receptor known as S1PR1, which is the receptor most important for mediating growth and migration through S1P signaling. In addition, the subcellular expression of the sphingosine kinases is altered in pancreatic cancer cells, which may contribute to their malignant behavior. Exogenous S1P increases pancreatic cancer cell migration, while inhibition of S1P signaling decreases the metabolic activity of pancreatic cancer cells as well as their ability to invade and migrate. Taken together, these results demonstrate the importance of S1P signaling in maintaining malignant behavior in pancreatic cancer cells. In addition, inhibition of S1P signaling represents a potential therapeutic target in pancreatic ductal cancer.
Type:
text; Electronic Thesis
Keywords:
pancreatic cancer; sphingosine-1-phosphate; sphingosine kinase; Medical Sciences; fingolimod
Degree Name:
M.S.
Degree Level:
masters
Degree Program:
Graduate College; Medical Sciences
Degree Grantor:
University of Arizona
Advisor:
Heimark, Ronald

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleSphingosine-1-Phosphate in Pancreatic Ductal Adenocarcinomaen_US
dc.creatorCardenas, Alexen_US
dc.contributor.authorCardenas, Alexen_US
dc.date.issued2013-
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractPancreatic ductal adenocarcinoma is an extremely lethal cancer that is difficult to treat. A better understanding of the biology of pancreatic ductal cancer will help to develop targeted therapies that may improve clinical outcomes. Recently, the lipid signaling molecule sphingosine-1-phosphate (S1P) has emerged as a driver of malignant behavior in many types of cancer. Its role in pancreatic cancer remains unknown. Pancreatic cancer cells express high levels of the S1P receptor known as S1PR1, which is the receptor most important for mediating growth and migration through S1P signaling. In addition, the subcellular expression of the sphingosine kinases is altered in pancreatic cancer cells, which may contribute to their malignant behavior. Exogenous S1P increases pancreatic cancer cell migration, while inhibition of S1P signaling decreases the metabolic activity of pancreatic cancer cells as well as their ability to invade and migrate. Taken together, these results demonstrate the importance of S1P signaling in maintaining malignant behavior in pancreatic cancer cells. In addition, inhibition of S1P signaling represents a potential therapeutic target in pancreatic ductal cancer.en_US
dc.typetexten_US
dc.typeElectronic Thesisen_US
dc.subjectpancreatic canceren_US
dc.subjectsphingosine-1-phosphateen_US
dc.subjectsphingosine kinaseen_US
dc.subjectMedical Sciencesen_US
dc.subjectfingolimoden_US
thesis.degree.nameM.S.en_US
thesis.degree.levelmastersen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplineMedical Sciencesen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorHeimark, Ronalden_US
dc.contributor.committeememberHeimark, Ronalden_US
dc.contributor.committeememberOng, Evanen_US
dc.contributor.committeememberJie, Tunen_US
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