Advanced-stage breast tumors have a high concentration of tumor necrosis factor-α (TNFα) throughout the tumor/stroma milieu, prompting sustained release of diverse chemokines (i.e.
In this study, hyaluronic acid (HA)-mediated tumor targeting and pH-sensitive amphiphilic polymeric nanoparticles were designed and prepared to co-deliver the anticancer drug embelin (EMB) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) plasmid (pTRAIL) (EMB/TRAIL-HA/PBAE-PEI) for synergistic anti-breast cancer efficacy.
Considering also the different inhibitory effects of the two drugs on TNF-α gene expression and NF-κB DNA-binding, the tuning of their combined delivery to the A375 tumor cell line might open a promising scenario for future therapeutic applications devoted to defeat human melanoma.
In vitro studies demonstrated that increased expression of CD62L by MDSCs was mediated by TNFα, elevated concentrations of which were found in tumor mice subjected to chronic inflammation.
An increased level of proinflammatory cytokines, including TNF-α in tumor microenvironment regulates the bioenergetic capacity, immune evasion and survival of cancer cells.
Biochemically, nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), reductive glutathione (GSH), and tumorTNF-α levels were measured in the testis.Serum TNF-α levels were also measured.
When administered to <i>Cynomolgus</i> monkey as intravenous injection, IL2-XE114-TNF<sup>mut</sup> showed the expected plasma concentration of ~1,500 ng/ml at early time points, indicating the absence of any <i>in vivo</i> trapping events, and a half-life of ~2 h. IL2-XE114-TNF<sup>mut</sup> may thus be considered as a promising biopharmaceutical for the treatment of metastatic clear-cell renal cell carcinoma, since these tumors are known to be sensitive to IL2 and to TNF.
The protective effect of GSK'963 did not affect the selective localization of the immunocytokine to tumors as evidenced by quantitative biodistribution analysis and allowed to reach high local TNF concentrations around tumor blood vessels, causing diffused vascular shutdown and hemorrhagic necrosis within the neoplastic mass.
Our findings show that cell survival genes mediated by TNF/TNFR2 binding is up-regulated in GC favoring its pro-tumoral effect, while pro-apoptotic genes as CASP3 and TNFR1 are down-regulated, indicating disbalance between apoptosis and cell proliferation processes in this neoplasm.
Targeting TRAIL (Tumor necrosis factor (TNF)-Related Apoptosis-Inducing Ligand) receptors for cancer therapy remains challenging due to tumor cell resistance and poor preparations of TRAIL or its derivatives.
Either Sal-B or cisplatin treatment decreased tumor tissue levels of tumor necrosis factor (TNF-α), matrix metalloproteinase-8 (MMP-8), and Cyclin D1 in ESC treated mice.
We showed that AT EC exposed in vitro to TGF-β (tumor growth factor-β), TNF-α (tumor necrosis factor-α), and IFN-γ (interferon-γ) undergo EndoMT with progressive loss of endothelial markers.
Mu-2-related death-inducing gene (MUDENG, <i>MuD</i>) has been reported to be involved in the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-associated apoptotic pathway of glioblastoma multiforme (GBM) cells; however, its expression level, interactors, and role in tumors are yet to be discovered.
Although the antibody fusion with TNF mediated a rapid hemorrhagic necrosis of the tumor mass, a slower regression of the neoplastic lesions (which continued after the last injection) was observed with the other fusion proteins, and treated mice acquired protective anticancer immunity.
The antibody-based delivery of certain proinflammatory payloads (such as IL2, IL12, and TNF) to the tumor microenvironment can lead to a dramatic potentiation of their anticancer activity.