Locally Targeting the IL-17/IL-17RA Axis Reduced Tumor Growth in a Murine B16F10 Melanoma Model

2019 ◽  
Vol 30 (3) ◽  
pp. 273-285 ◽  
Author(s):  
Ya-Shan Chen ◽  
Tse-Hung Huang ◽  
Chao-Lin Liu ◽  
Hui-Shan Chen ◽  
Meng-Hua Lee ◽  
...  
Keyword(s):  
Tumor Growth ◽  
B16f10 Melanoma ◽  
Melanoma Model

Transforming growth factor-β1 inhibits tumor growth in a mouse melanoma model by down-regulating the plasminogen activation system

2003 ◽  
Vol 291 (1) ◽  
pp. 1-10 ◽  
Author(s):  
Laurent Ramont ◽  
Sylvie Pasco ◽  
William Hornebeck ◽  
François-Xavier Maquart ◽  
Jean Claude Monboisse
Keyword(s):  
Growth Factor ◽  
Tumor Growth ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Plasminogen Activation ◽  
Mouse Melanoma ◽  
Plasminogen Activation System ◽  
Activation System ◽  
Mouse Melanoma Model ◽  
Melanoma Model

scholarly journals Effects of N-acetyl-glucosamine-coated glycodendrimers as biological modulators in the B16F10 melanoma model in vivo

2014 ◽  
Vol 44 (4) ◽  
pp. 1410-1410 ◽  
Author(s):  
LUCA VANNUCCI ◽  
ANNA FISEROVÁ ◽  
KASHINATH SADALAPURE ◽  
THISBE K. LINDHORST ◽  
MARKETA KULDOVÁ ◽  
...  
Keyword(s):  
B16f10 Melanoma ◽  
Melanoma Model

Chrysin, a natural and biologically active flavonoid suppresses tumor growth of mouse B16F10 melanoma cells: In vitro and In vivo study

2018 ◽  
Vol 283 ◽  
pp. 10-19 ◽  
Author(s):  
Aïcha Sassi ◽  
Mouna Maatouk ◽  
Dorra El gueder ◽  
Imen Mokdad Bzéouich ◽  
Saïda Abdelkefi-Ben Hatira ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Melanoma Cells ◽  
Biologically Active ◽  
In Vivo Study ◽  
B16f10 Melanoma ◽  
B16f10 Melanoma Cells

Abstract 442: Decreased tumor progression by the knockdown of interleukin 17 receoptor A in the B16F10 melanoma model

2015 ◽  
Author(s):  
Ya-Shan Chen ◽  
Chao-Lin Liu ◽  
Hui-Shan Chen ◽  
Su-Ting Wu ◽  
Chia-Rui Shen
Keyword(s):  
Tumor Progression ◽  
Interleukin 17 ◽  
B16f10 Melanoma ◽  
Melanoma Model

Abstract A79: Inhibition of p53-MDM2 protein interaction reduces tumor growth in a mouse melanoma model

2020 ◽  
Author(s):  
Katrine Ingelshed ◽  
Danai Lianoudaki ◽  
Dilraj Lama ◽  
Silke Sohn ◽  
Nicolas Fritz ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Protein Interaction ◽  
Mdm2 Protein ◽  
Mouse Melanoma ◽  
Mouse Melanoma Model ◽  
Melanoma Model

Effects of N-acetyl-glucosamine-coated glycodendrimers as biological modulators in the B16F10 melanoma model in vivo

2003 ◽  
Author(s):  
Luca Vannucci ◽  
Anna Fiserová ◽  
Kashinath Sadalapure ◽  
Thisbe Lindhorst ◽  
Marketa Kuldová ◽  
...  
Keyword(s):  
B16f10 Melanoma ◽  
Melanoma Model

Mangiferin, a novel nuclear factor kappa B-inducing kinase inhibitor, suppresses metastasis and tumor growth in a mouse metastatic melanoma model

2016 ◽  
Vol 306 ◽  
pp. 105-112 ◽  
Author(s):  
Tomoya Takeda ◽  
Masanobu Tsubaki ◽  
Kotaro Sakamoto ◽  
Eri Ichimura ◽  
Aya Enomoto ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Metastatic Melanoma ◽  
Nuclear Factor Kappa B ◽  
Kinase Inhibitor ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Melanoma Model

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.

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