scholarly journals Expression of the fusogenic p14 FAST protein from a replication-defective adenovirus vector does not provide a therapeutic benefit in an immunocompetent mouse model of cancer

2016 ◽  
Vol 23 (10) ◽  
pp. 355-364 ◽  
Author(s):  
C M Wong ◽  
L A Nash ◽  
J Del Papa ◽  
K L Poulin ◽  
T Falls ◽  
...  
1995 ◽  
Vol 69 (10) ◽  
pp. 6180-6190 ◽  
Author(s):  
A Fujita ◽  
K Sakagami ◽  
Y Kanegae ◽  
I Saito ◽  
I Kobayashi

Author(s):  
Hai-Jun Hu ◽  
Xiu Liang ◽  
Hai-Lang Li ◽  
Huai-Yuan Wang ◽  
Jin-Fa Gu ◽  
...  

AbstractAlthough the recent treatment in melanoma through the use of anti-PD-1 immunotherapy is successful, the efficacy of this approach remains to be improved. Here, we explore the feasibility of combination strategy with the armed oncolytic adenovirus ZD55-IL-24 and PD-1 blockade. We find that combination therapy with localized ZD55-IL-24 and systemic PD-1 blockade leads to synergistic inhibition of both local and distant established tumors in B16-bearing immunocompetent mouse model. Our further mechanism investigation reveals that synergistic therapeutic effect is associated with marked promotion of tumor immune infiltration and recognition in both local and distant tumors as well as spleens. PD-1 blockade has no obvious effect on promotion of tumor immune infiltration and recognition. Localized therapy with ZD55-IL-24, however, can help PD-1 blockade to overcome the limitation of relatively low tumor immune infiltration and recognition. This study provides a rationale for investigation of such combination therapy in the clinic.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Lucy J. Newbury ◽  
Jui-Hui Wang ◽  
Gene Hung ◽  
Bruce M. Hendry ◽  
Claire C. Sharpe

Abstract Chronic Kidney Disease is a growing problem across the world and can lead to end-stage kidney disease and cardiovascular disease. Fibrosis is the underlying mechanism that leads to organ dysfunction, but as yet we have no therapeutics that can influence this process. Ras monomeric GTPases are master regulators that direct many of the cytokines known to drive fibrosis to downstream effector cascades. We have previously shown that K-Ras is a key isoform that drives fibrosis in the kidney. Here we demonstrate that K-Ras expression and activation are increased in rodent models of CKD. By knocking down expression of K-Ras using antisense oligonucleotides in a mouse model of chronic folic acid nephropathy we can reduce fibrosis by 50% and prevent the loss of renal function over 3 months. In addition, we have demonstrated in vitro and in vivo that reduction of K-Ras expression is associated with a reduction in Jag1 expression; we hypothesise this is the mechanism by which targeting K-Ras has therapeutic benefit. In conclusion, targeting K-Ras expression with antisense oligonucleotides in a mouse model of CKD prevents fibrosis and protects against renal dysfunction.


PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0122387 ◽  
Author(s):  
Benjamin H. Beck ◽  
Hyunggoon Kim ◽  
Rebecca O’Brien ◽  
Martin R. Jadus ◽  
G. Yancey Gillespie ◽  
...  

2017 ◽  
Vol 19 (suppl_6) ◽  
pp. vi78-vi78 ◽  
Author(s):  
Braden McFarland ◽  
Kory Dees ◽  
Nathalia Melo ◽  
Samuel Fehling ◽  
Sara Gibson ◽  
...  

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