Browsing by Author "Johnston, Randal N."
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- ItemOpen AccessCellular adaptations to gene amplification(1993) Lintott, Lauri; Johnston, Randal N.
- ItemOpen AccessControlled amplification of c-myc proto-oncogene in Chinese hampster ovary cells(1991) Cheng, Ting; Johnston, Randal N.
- ItemOpen AccessDiverse genome structures of Salmonella paratyphi C(BioMed Central, 2007-08-27) Liu, Wei-Qiao; Liu, Gui-Rong; Li, Jun-Qian; Xu, Guo-Min; Qi, Danni; He, Xiao-Yan; Deng, Juan; Zhang, Feng-Min; Johnston, Randal N.; Liu, Shu- Lin
- ItemOpen AccessEstrogen regulation of C-MYC gene expression in proliferating chick oviduct(1990) Rempel, Sandra A.; Johnston, Randal N.
- ItemOpen AccessGoing (Reo)viral: factors promoting successful revival oncolytics infection(MDPI, 2018-08-11) Bourhill, Tarryn; Mori, Yoshinori; Rancourt, Derrick Emile; Shmulevitz, Maya; Johnston, Randal N.Oncolytic viruses show intriguing potential as cancer therapeutic agents. These viruses are capable of selectively targeting and killing cancerous cells while leaving healthy cells largely unaffected. The use of oncolytic viruses for cancer treatments in selected circumstances has recently been approved by the Food and Drug Administration (FDA) of the US and work is progressing on engineering viral vectors for enhanced selectivity, efficacy and safety. However, a better fundamental understanding of tumour and viral biology is essential for the continued advancement of the oncolytic field. This knowledge will not only help to engineer more potent and effective viruses but may also contribute to the identification of biomarkers that can determine which patients will benefit most from this treatment. A mechanistic understanding of the overlapping activity of viral and standard chemotherapeutics will enable the development of better combinational approaches to improve patient outcomes. In this review, we will examine each of the factors that contribute to productive viral infections in cancerous cells versus healthy cells. Special attention will be paid to reovirus as it is a well-studied virus and the only wild-type virus to have received orphan drug designation by the FDA. Although considerable insight into reoviral biology exists, there remain numerous deficiencies in our understanding of the factors regulating its successful oncolytic infection. Here we will discuss what is known to regulate infection as well as speculate about potential new mechanisms that may enhance successful replication. A joint appreciation of both tumour and viral biology will drive innovation for the next generation of reoviral mediated oncolytic therapy.
- ItemOpen AccessMechanisms of resistance to reoviral oncolysis(2005) Kim, Manbok; Johnston, Randal N.
- ItemOpen AccessModulation of c-fos gene expression by amplification(1993) Wong, Howard; Johnston, Randal N.
- ItemOpen AccessMolecular analyses of cellular replicative senescence(1995) Atadja, Peter Wisdom; Johnston, Randal N.; Riabowol, Karl T.
- ItemOpen AccessMultiple genetic switches spontaneously modulating bacterial mutability(BioMed Central, 2010-09-13) Chen, Fang; Liu, Wei-Qiao; Eisenstark, Abraham; Johnston, Randal N.; Liu, Gui-Rong; Liu, Shu-Lin
- ItemOpen AccessRegulation of endo-B-Mannanase production in isolated endosperms from seeds of Lactuca sativa C.V. Grand Rapids(1987) Dulson, Jacqueline; Johnston, Randal N.
- ItemOpen AccessRegulation of metallothionein gene expression in Chinese hamster ovary cells(1989) Dutler, Sarah M. L.; Johnston, Randal N.
- ItemOpen AccessReoviral Cytolysis is Modulated by Stemness(2020-10-13) Bourhill, Tarryn Jackie; Johnston, Randal N.; Rancourt, Derrick E.; Cobb, Jennifer A.; Mahoney, Douglas J.Oncolytic viruses (OVs) are an emerging cancer therapeutic that act by selectively targeting and lysing cancerous cells and by stimulating anti-tumour immune responses, while leaving normal cells mainly unaffected. Reovirus is a well-studied OV that received fast track designation and a special protocol assessment agreement from the FDA for the treatment of metastatic breast cancer. The mechanisms governing reoviral selectivity are not well characterised and are a topic of debate. Reovirus is capable of infecting and lysing cancer cells and, cancer stem cells, and here we demonstrate its ability to also infect and kill healthy pluripotent stem cells (PSCs). This has led us to hypothesize that pathways responsible for stemness modulate reoviral tropism. We find that reovirus is capable of killing murine and human embryonic and induced pluripotent stem cells. Differentiation of PSCs alters the cells’ reoviral-permissive state to a resistant one. In a cancer cell line that was resistant to reoviral oncolysis, induction of pluripotency programming renders these cells permissive to cytolysis. In light of the recent view that pluripotency induction shares similar pathways with carcinogenesis, the same subset of genes that are activated in cancer may also be up-regulated in PSCs (e.g. c-MYC), rendering PSCs permissive to infection. Bioinformatic analysis indicated that the Yamanaka factors may be involved in regulating reoviral selectivity, however this requires further experimental validation. Mechanistic insights from these studies will be useful for the advancement of reoviral oncolytic therapy.
- ItemOpen AccessSPC-P1: a pathogenicity-associated prophage of Salmonella paratyphi C(BioMed Central, 2010-12-30) Zou, Qing-Hua; Li, Qing-Hai; Zhu, Hong-Yun; Feng, Ye; Li, Yong-Guo; Johnston, Randal N.; Liu, Gui-Rong; Liu, Shu-Lin
- ItemOpen AccessThe measurement of c-fos mRNA stability(1999) Pinchbeck, Geoffrey George; Johnston, Randal N.
- ItemOpen AccessTranslational control during neuronal differentiation(1994) Xu, Wanting; Johnston, Randal N.