Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We found that glioblastoma resistance to gefitinib may be mediated by an adaptive pro-survival TNFα-JNK-Axl signaling axis, and that high TNFα levels in the glioblastoma microenvironment may further intensify primary resistance.
|
31565489 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Human mesenchymal stem cell (MSC)-based tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) gene delivery is regarded as an effective treatment for glioblastoma (GBM).
|
30867058 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we compare the efficacy of TMZ versus EGFR plus TNF inhibition in an orthotopic mouse model of GBM.
|
31363754 |
2019 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Treatment of human U251 and TG1 glioblastoma cells with both flavonoids also modulated negatively the expression of mRNA for IL-6 and IL-10 and positively the expression of mRNA for TNF characterizing changes to the immune regulatory profile.
|
31059805 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
The tumor necrosis factor receptor CD40 and its ligand CD40L have shown value as biomarkers for GBM.
|
31125770 |
2019 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Additionally, TP53 GOF mutation and CCL2 and TNFA expression correlated positively with tumor-associated immunity in patients with GBM.
|
29786075 |
2019 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In addition, by pretreating hAMSCs expression of tumor necrosis factor-related apoptosis-inducing ligand with TGF-β, we achieved significant enhancements in the therapeutic efficacy as demonstrated by an increased number of migrated hAMSCs to target sites, decreased tumor volume, and prolonged survival time in a murine model of GBM.
|
30863846 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
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.
|
31616474 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
GBM cells are frequently resistant to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and finding new combinatorial therapies to sensitize glioma cells to TRAIL remains an important challenge.
|
30718520 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Treatment of GBM cells with MC4040 and MC4041 also impaired the GBM pro-inflammatory phenotype, with a significant decrease of TGF-β, TNF-α, and IL-6, joined to an increase of the anti-inflammatory cytokine IL-10.
|
31791385 |
2019 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
We created constitutive and regulatable miR-7 expression vectors and utilized pharmacological inhibition of caspases and genetic loss of function to study the effect of forced expression of miR-7 on death receptor (DR) pathways in a cohort of GBM with established resistance to tumor necrosis factor apoptosis inducing ligand (TRAIL) and in patient-derived primary GBM stem cell (GSC) lines.
|
29016934 |
2018 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The TNF receptor superfamily member Fn14 is overexpressed by many solid tumor types, including glioblastoma (GBM), the most common and lethal form of adult brain cancer.
|
29453678 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our prior work has demonstrated an important role for the tumor necrosis factor-like weak inducer of apoptosis (TWEAK) receptor fibroblast growth factor-inducible 14 (Fn14) in GBM pathobiology.
|
29897522 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Peripheral blood from 205 treatment-naïve patients with glioma (GBM = 145; non-GBM = 60) was obtained on the day of surgery to measure (i) circulating T-cells reacting to viral antigens and TAAs, in the presence or absence of cytokine conditioning with IL-2/IL-15/IL-21 or IL-2/IL-7, and (ii) serum cytokine levels (IL-4, IL-5, IL-6, TNF-α, IFN-γ and IL-17A).
|
30049387 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, our data identified MAPK-ERK-YAP signaling pathways as the primary molecular mechanisms by which TNFα modulated mitochondrial fission and glioblastoma apoptosis.
|
30425514 |
2018 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We identified that CD44, ATP binding cassette subfamily C member 3 (ABCC3), and tumor necrosis factor receptor subfamily member 1A (TNFRSF1A) as highly expressed genes in GBMs are associated with patients' poor outcomes and therapy resistance.
|
30341039 |
2018 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings provide a possible explanation for the failures of anti-EGFR therapy in GBM and suggest a new approach to the treatment of EGFR-expressing GBM using a combination of EGFR and TNF inhibition.
|
28604685 |
2017 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Serial imaging showed that h-iNSC<sup>TE</sup> delivery of the proapoptotic agent tumor necrosis factor-α-related apoptosis-inducing ligand (TRAIL) reduced the size of solid human GBM xenografts 250-fold in 3 weeks and prolonged median survival from 22 to 49 days.
|
28148846 |
2017 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of NF-κB Pathway and Modulation of MAPK Signaling Pathways in Glioblastoma and Implications for Lovastatin and Tumor Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL) Combination Therapy.
|
28135339 |
2017 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Activation of NF-κB by TNFα decreases calcium induced mPTP opening, elevates mitochondrial potential and increases reactive oxygen species (ROS) production in both T98G human glioblastoma cells and rat cortical neurons.
|
28317877 |
2017 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
We recently reported that mammalian target of rapamycin inhibitors-rapamycin, temsirolimus, torin 1, and PP242-suppressed invasion and migration promoted by tumor necrosis factor-alpha and phorbol-myristate-acetate in glioblastoma cells.
|
28351321 |
2017 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In in vitro study, HCMV infection induced the expression of interleukin 6 and tumor necrosis factor-α in human glioblastoma U87 MG (U87) cells and human umbilical vein endothelial cells (HUVECs).
|
27474433 |
2016 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
The highest mean values of PHLPP1 mRNA and protein were found in non-glioma brain tissues whereas the lowest mean values were found in those in glioblastoma with an increase of TNF-α, IL-17, IL-1β (p<0.05).
|
26971226 |
2016 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
These observations demonstrate that olive oil compounds inhibit the effect of the chronic inflammatory microenvironment on glioblastoma progression through TNF-α actions and may be useful in cancer chemoprevention.
|
26410343 |
2016 |
Glioblastoma Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Glioblastoma microenvironment contains high levels of TNFα and IL-1β, which mediate inflammation through induction of a local network of cytokines and chemokines.
|
26794430 |
2016 |