Articles by Thomas M.B. Ware in JoVE
Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System Hao Chen*1, Thomas M.B. Ware*1, Josephine Iaria1, Hong-Jian Zhu1 1Department of Surgery (RMH), University of Melbourne Here, we present a protocol for live cell imaging of TGF-β/Smad3 signaling activity using an adenovirus reporter system. This system tracks transcriptional activity in real-time and can be applied to both single cells in vitro and in live animalmodels.
Other articles by Thomas M.B. Ware on PubMed
Mouse Models of Glioma Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia. Apr, 2015 | Pubmed ID: 25698543 Gliomas are the most common primary tumour in the central nervous system in adults. The pathological hallmark of gliomas is their propensity for extensive infiltration into the surrounding brain parenchyma which results in tumour recurrence. Despite the use of optimal surgical removal and adjuvant therapies the most aggressive of these tumours, glioblastoma multiforme, has a poor patient prognosis, with median survival of less than 15 months. In this review, we discuss mouse glioma models that have been utilised to advance our basic knowledge of the processes involved in gliomagenesis and their use in the testing of novel therapies and treatment regimens in the preclinical setting.
Inhibition of Glioblastoma Cell Proliferation, Migration and Invasion by the Proteasome Antagonist Carfilzomib Medical Oncology (Northwood, London, England). May, 2016 | Pubmed ID: 27098175 Glioblastoma multiforme is the most aggressive and lethal tumor of the central nervous system with limited treatment strategies on offer, and as such the identification of effective novel therapeutic agents is paramount. To examine the efficacy of proteasome inhibitors, we tested bortezomib, carfilzomib, nafamostat mesylate, gabexate mesylate and acetylsalicylic acid on glioblastoma cell viability, migration and invasion. Both bortezomib and carfilzomib produced significant reduction of cell viability, while nafamostat mesylate, gabexate mesylate and acetylsalicylic acid did not. Subsequent testing showed that carfilzomib significantly reduced cell viability at nM concentrations. Carfilzomib also reduced cell migration, secretion and activation of MMP2 and also cell invasion of all four glioblastoma cells tested. In summary, carfilzomib represents a novel, yet FDA-approved agent for the treatment of glioblastoma multiforme.