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Utilizing Positron Emission Tomography to Detect Functional Changes Following Drug Therapy in a Renal Cell Carcinoma Mouse Model Open Access


Other title
tyrosine kinase inhibitor
renal cell carcinoma
positron emission tomography
Type of item
Degree grantor
University of Alberta
Author or creator
Chapman, David W
Supervisor and department
Moore, Ronald (Surgery)
Examining committee member and department
Moore, Ronald (Surgery)
Zemp, Roger (Electrical Engineering)
Wiebe, Leonard (Oncology)
Wuest, Melinda (Oncology)
Department of Surgery
Experimental Surgery
Date accepted
Graduation date
Master of Science
Degree level
Sunitinib is currently the first line drug therapy for metastasizing renal cell carcinoma (RCC). It has been shown to have a profound effect on tumor angiogenesis leading to modifications of the tumor’s microenvironment. Tumor hypoxia plays an important role in the metastatic potential of a solid tumor and its resistance to any chemotherapy. Therefore, monitoring tumor hypoxia could potentially be used to detect and analyze therapeutic response. The present study utilized Positron-Emission Tomography (PET) to determine changes in tumor oxygenation during and following sunitinib therapy in a mouse RCC tumor model. Uptake of [18F]FAZA tended to decrease during therapy of sunitinib, indicating a decrease in the tumor’s hypoxia. However, after stopping drug therapy in tumor-bearing mice, this effect was reversed and tumor hypoxia was increased. [18F]FAZA could potentially be used to monitor drug response of sunitinib therapy for RCC.
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