Sentence examples for mouse melanoma model from inspiring English sources
UV-induced somatic mutations elicit a functional T cell response in the YUMMER1.7 mouse melanoma model.
Perna, D. et al. BRAF inhibitor resistance mediated by the AKT pathway in an oncogenic BRAF mouse melanoma model.
Heller L, Merkler K, Westover J, Cruz Y, Coppola D, Benson K, et al. Evaluation of toxicity following electrically mediated interleukin-12 gene delivery in a B16 mouse melanoma model.
Compound 7 also demonstrated significant in vivo inhibition of tumor growth and angiogenesis in a B16-F10 syngeneic mouse melanoma model.
Importantly, enhanced activity of high-AR aAPCs was seen in a mouse melanoma model, with high-AR aAPCs improving melanoma survival compared to non-cognate aAPCs (p = 0.004) and cognate spherical aAPCs (p = 0.05).
The purpose of this study was to engineer canine AT-MSC (cAT-MSC) producing IFN-β and to evaluate the anti-tumor effect of cAT-MSC IFN-β cAT-MSC IFN-β cAT-MSC IFN-βmouse melanoma model.
Using mouse melanoma models, we report that CD8 TILs enhance peroxisome proliferator-activated receptor (PPAR -α signaling and catabolism of fatty acids (FAs) when simultaneously subjected to hyPPAR -αmia and hypoxia.
Future studies using mouse melanoma models will be required to assess both the anti-tumor activity and toxicity of our proposed combination therapy in vivo.
Additionally, mutations in the amino acid sequence of LRP2, altered function of MAP2K1 and MAP2K2 induced by genetic mutations in melanoma patients [ 17], and mutations in GRM5 in mouse melanoma models [ 20] were also reported.
Targeting antigens via DEC-205 into DC showed promising results in various mouse melanoma models in that melanoma-associated antigens conjugated to anti-DEC-205 slowed down tumor growth 55, 56.
Recently, Lannone et al. reported that combination treatment with both APCP and anti-CTLA-4 mAb displayed significant retard of tumor growth compared with APCP or anti-CTLA-4 mAb treatment alone in mouse melanoma models [ 74].
