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dc.contributor.advisorHiss, Donavon
dc.contributor.advisorFlepisi, Brian
dc.contributor.authorRoos, Kelly
dc.date.accessioned2021-03-09T10:36:25Z
dc.date.available2021-03-09T10:36:25Z
dc.date.issued2020
dc.identifier.urihttp://hdl.handle.net/11394/7952
dc.descriptionMagister Scientiae (Medical Bioscience) - MSc(MBS)en_US
dc.description.abstractCancer is a global health catastrophe, with neuroblastoma, the most common solid childhood tumor, and glioblastoma, a deadly brain tumor, being aggressive and unresponsive to current treatment modalities. These tumors are known to utilize uncontrollable cell proliferative capabilities as a mechanism for tumor survival. Therefore, malignant cell growth can be mitigated by targeting the essential proteins that regulate cell growth, such as receptor tyrosine kinases (RTKs). Under normal physiological conditions, RTKs bind with varying affinity to mitogenic stimuli such as growth factors such as vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) which, in turn, leads to receptor phosphorylation and activation.en_US
dc.publisherUniversity of the Western Capeen_US
dc.subjectSunitiniben_US
dc.subjectNeuroblastomaen_US
dc.subjectReceptor tyrosine kinasesen_US
dc.subjectTyrosine kinase inhibitorsen_US
dc.subjectVascular endothelial growth factoren_US
dc.titleThe effect of sunitinib on neuroblastoma and glioblastoma cell growthen_US
dc.rights.holderUniversity of the Western Capeen_US


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