IFN-β-Dependent Inhibition of Tumor Growth by the Vascular Disrupting Agent 5,6-Dimethylxanthenone-4-Acetic Acid (DMXAA)

2008 ◽  
Vol 28 (3) ◽  
pp. 133-139 ◽  
Author(s):  
Zachary J. Roberts ◽  
Lai-Ming Ching ◽  
Stefanie N. Vogel
Keyword(s):  
Acetic Acid ◽  
Tumor Growth ◽  
Vascular Disrupting Agent ◽  
Dependent Inhibition ◽  
Inhibition Of Tumor Growth ◽  
Vascular Disrupting

Primary tumor dependent inhibition of tumor growth, angiogenesis, and perfusion of secondary breast cancer in bone

2011 ◽  
Vol 29 (8) ◽  
pp. 1251-1258 ◽  
Author(s):  
Christian Schaefer ◽  
Malte Schroeder ◽  
Ina Fuhrhop ◽  
Lennart Viezens ◽  
Jasmin Otten ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Primary Tumor ◽  
Dependent Inhibition ◽  
Inhibition Of Tumor Growth ◽  
Secondary Breast Cancer

scholarly journals Activity of the Vascular-Disrupting Agent 5,6-Dimethylxanthenone-4-Acetic Acid against Human Head and Neck Carcinoma Xenografts

Neoplasia ◽  
2006 ◽  
Vol 8 (7) ◽  
pp. 534-542 ◽  
Author(s):  
Mukund Seshadri ◽  
Richard Mazurchuk ◽  
Joseph A. Spernyak ◽  
Arup Bhattacharya ◽  
Youcef M. Rustum ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Head And Neck ◽  
Head And Neck Carcinoma ◽  
Human Head ◽  
Vascular Disrupting Agent ◽  
Neck Carcinoma ◽  
Vascular Disrupting

scholarly journals Vascular disrupting agent induced aggregation of gold nanoparticles for photothermally enhanced tumor vascular disruption

2020 ◽  
Vol 6 (23) ◽  
pp. eabb0020 ◽  
Author(s):  
Sheng Hong ◽  
Di-Wei Zheng ◽  
Cheng Zhang ◽  
Qian-Xiao Huang ◽  
Si-Xue Cheng ◽  
...  
Keyword(s):  
Gold Nanoparticles ◽  
Tumor Growth ◽  
Tumor Therapy ◽  
Tumor Model ◽  
Vascular Damage ◽  
Photothermal Effect ◽  
Tumor Growth Inhibition ◽  
Vascular Disrupting Agent ◽  
Induced Aggregation ◽  
Vascular Disrupting

Although vascular disrupting agents (VDAs) have been extensively implemented in current clinical tumor therapy, the notable adverse events caused by long-term dosing severely limit the therapeutic efficacy. To improve this therapy, we report a strategy for VDA-induced aggregation of gold nanoparticles to further destroy tumor vascular by photothermal effect. This strategy could effectively disrupt tumor vascular and cut off the nutrition supply after just one treatment. In the murine tumor model, this strategy results in notable tumor growth inhibition and gives rise to a 92.7% suppression of tumor growth. Besides, enhanced vascular damage could also prevent cancer cells from distant metastasis. Moreover, compared with clinical therapies, this strategy still exhibits preferable tumor suppression and metastasis inhibition ability. These results indicate that this strategy has great potential in tumor treatment and could effectively enhance tumor vascular damage and avoid the side effects caused by frequent administration.

Combinatorial treatment with CTO and temozolomide in sc-implanted human LOX 1MVI melanoma.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e19006-e19006
Author(s):  
Rashida A. Karmali ◽  
Yulia Maxuitenko ◽  
Greg Gorman
Keyword(s):  
Antitumor Activity ◽  
Tumor Growth ◽  
Calcium Influx ◽  
Dependent Inhibition ◽  
Melanoma Model ◽  
Dose Dependent Inhibition ◽  
Inhibition Of Tumor Growth ◽  
Induction Of Apoptosis ◽  
Oxide Synthase ◽  
Dose Dependent

e19006 Background: Carboxyamidotriazole orotate (CTO) is the orotic acid salt of 5-amino-1.(4-(4-chlorobenzoyl)-3,5-dichlorobenzyl)-1, 2, 3-triazole-4-carboxamide. CTO possesses increased solubility. The antiproliferative and antimetastatic effects of CTO are related to inhibition of receptor –opertated calcium channel- mediated calcium influx. CTO can inhibit calcium sensitive signal transduction in the VEGF and the PI3K pathways, inhibition of FGF-2-induced tyrosine kinase, VEGF-mediated activation of phospholipase Cγ, generation of IP3 and nitric oxide synthase activation, and induction of apoptosis in imatinib mesylate resistant CML cells by downregulating bcr-abl. Methods: Different combinations of CTO and temozolomide (TEM) were first tested in female athymic NCr-nu/nu mice to evaluate tolerance of the combination. The tolerated combinations were then tested to evaluate the antitumor activity against subcutaneously –implanted human LOX 1MVI melanoma xenografts. Results: Oral CTO at doses of 513 or 342 mg/kg/dose Q1Dx14 resulted in inhibition of tumor growth (p<0.001 and p=0.004). Oral TEM at doses of 90 and 60mg/kg/dose Q4Dx3 resulted in dose-dependent inhibition of tumor growth (p<0.001 and p<0.001). Oral CTO at 513 or 342 mg/kg/dose in combination with TEM 90mg/kg/dose resulted in comparable tumor inhibition to TEM alone. However, oral CTO at 513mg/kg/dose in combination with TEM 60mg/kg/dose resulted in additive antitumor activity compared to each drug alone. Also, CTO at 342mg/kg/dose in combination with TEM 60mg/kg/dose had more than additive antitumor activity and was statistically different from the group treated with TEM 60mg/kg/dose alone (p=0.001). Conclusions: These results suggest that CTO enhances the sensitivity of TEM and may permit use of lower doses of TEM to obtain an optimum antitumor effect in combination therapy thus reducing toxicity of high TEM doses in this melanoma model.

scholarly journals Isotype-Dependent Inhibition of Tumor Growth In Vivo by Monoclonal Antibodies to Death Receptor 4

2001 ◽  
Vol 166 (8) ◽  
pp. 4891-4898 ◽  
Author(s):  
Anan Chuntharapai ◽  
Kelly Dodge ◽  
Katharine Grimmer ◽  
Kurt Schroeder ◽  
Scot A. Marsters ◽  
...  
Keyword(s):  
Monoclonal Antibodies ◽  
Tumor Growth ◽  
Death Receptor ◽  
Dependent Inhibition ◽  
Inhibition Of Tumor Growth ◽  
Death Receptor 4

scholarly journals 5,6-Dimethylxanthenone-4-Acetic Acid in the Treatment of Refractory Tumors: a Phase I Safety Study of a Vascular Disrupting Agent

2006 ◽  
Vol 12 (6) ◽  
pp. 1776-1784 ◽  
Author(s):  
Mark J. McKeage ◽  
Peter Fong ◽  
Mark Jeffery ◽  
Bruce C. Baguley ◽  
Phil Kestell ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Phase I ◽  
Safety Study ◽  
Vascular Disrupting Agent ◽  
Vascular Disrupting
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