|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Combination treatment of berberine and solid lipid curcumin particles increased cell death and inhibited PI3K/Akt/mTOR pathway of human cultured glioblastoma cells more effectively than did individual treatments.
|
31841506 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
For example, combining gefitinib with inhibitors of the PI3K/AKT pathway show enhanced cytotoxicity in glioblastoma derived cell lines.
|
18566746 |
2008 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Curcumin and Solid Lipid Curcumin Particles Induce Autophagy, but Inhibit Mitophagy and the PI3K-Akt/mTOR Pathway in Cultured Glioblastoma Cells.
|
30669284 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Given this disparity and to address the relation of patient age to mutation frequency, we examined 10 exons of PIK3CA in 73 glioblastoma samples by PCR amplification followed by direct DNA sequencing.
|
17050665 |
2006 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Using two different migration assays, Western blotting, conventional and super-resolution (dSTORM) fluorescence microscopy we examine the effects of the dual PI3K/mTOR-inhibitor PI-103 alone and in combination with the Hsp90 inhibitor NVP-AUY922 and/or irradiation on the migration, expression of marker proteins, focal adhesions and F-actin cytoskeleton in two GBM cell lines (DK-MG and SNB19) markedly differing in their invasive capacity.
|
28424411 |
2017 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The objective of this study was to examine whether PIK3CA mutations are associated with a specific clinical phenotype in glioblastoma.
|
31036078 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The phosphoinositide 3-kinase (PI3K) pathway is targeted for frequent alteration in glioblastoma (GBM) and is one of the core GBM pathways defined by The Cancer Genome Atlas.
|
23166678 |
2012 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
We have examined the relative roles of the two major phospholipid products of PI3K activity, phosphatidylinositol 3,4-biphosphate [PtdIns(3,4)P2] and phosphatidylinositol 3,4,5-triphosphate [PtdIns(3,4,5)P3], in the regulation of PKB activity in glioblastoma cells containing high levels of both of these lipids due to defective PTEN expression.
|
10958682 |
2000 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
The PI3K/AKT/mTOR pathway is commonly over activated in glioblastoma (GBM), and Rictor was shown to be an important regulator downstream of this pathway.
|
23555046 |
2013 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The phosphatase and tensin homolog (PTEN)/phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mTOR pathway has emerged as a crucial player in GBM development and progression.
|
30662577 |
2018 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Epidermal growth factor receptor (EGFR) mutations (EGFRvIII) and phosphoinositide 3-kinase (PI3K) hyperactivation are common in GBM, promoting tumor growth and survival, including through sterol regulatory element-binding protein 1 (SREBP-1)-dependent lipogenesis.
|
22059152 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Our study demonstrates, for the first time, that vaults have a tumour-promoting potential by stabilizing EGFR/PI3K-mediated migration and survival pathways in human glioblastoma.
|
24243798 |
2013 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Mechanistically, cPLA2α knockdown significantly suppresses the PI3K/Akt/mTOR pathway in glioblastoma cells.
|
30360807 |
2018 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, the current study demonstrated for the first time that inhibition of RWDD3 expression inhibited glioblastoma progression, at least partly, via suppressing the PI3K/AKT signaling activity, and thus RWDD3 may be a novel potential therapeutic target for glioblastoma.
|
29977365 |
2018 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Using single-cell tracking and wound healing migration tests, colony-forming assay, Western blotting, flow cytometry and electrorotation we examined the effects of MK-2206 and PI-103 and/or irradiation on the migration, radiation sensitivity, expression of several marker proteins, DNA damage, cell cycle progression and the plasma membrane properties in two glioblastoma (DK-MG and SNB19) cell lines, previously shown to differ markedly in their migratory behavior and response to PI3K/mTOR inhibition.
|
30943918 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Nevertheless, the administration of the dual PI3K/mTOR inhibitor BEZ235 potentiated the effect of TMZ plus MET on cell viability, inducing a pro-apoptotic phenotype during hypoxic condition also in T98 cells, suggesting the block of the PI3K/AKT/mTOR pathway as a complementary target to further overcome GBM resistance during hypoxia.
|
31214505 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Specifically, targeting cellular pathways frequently altered in glioblastoma, such as the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR), the p53 and the retinoblastoma (RB) pathways, or epidermal growth factor receptor (EGFR) gene amplification or mutation, have failed to improve outcome, likely because of redundant compensatory mechanisms, insufficient target coverage related in part to the blood brain barrier, or poor tolerability and safety.
|
31541850 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
These findings suggest that the PI3K/mTor signaling pathway is critical for the maintenance of glioblastoma CSLC properties, and targeting both mTor and PI3K of CSLCs may be an effective therapeutic strategy in glioblastoma.
|
20861085 |
2010 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
We previously developed a non-germline genetically engineered mouse model of GBM in which PI3K and MAPK are activated via Pten deletion and KrasG12D in immortalized astrocytes.
|
28379424 |
2017 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Additionally, we found no effect of the VRAC inhibition using siRNA treatment or DCPIB on PI3K/Akt signaling in glioblastoma cells.
|
31151189 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
This RTK/PTEN/PI3K pathway leads to activated AKT and phospho-AKT levels are elevated in the majority of GBM tumor samples and cell lines, which studies show help glioma cells grow uncontrolled, evade apoptosis, and enhance tumor invasion.
|
21827416 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The EGFR and PI3K/mTORC1/2 pathways are frequently altered in glioblastoma (GBM), but pharmacologic targeting of EGFR and PI3K signaling has failed to demonstrate efficacy in clinical trials.
|
25316808 |
2014 |
|
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Rapamycin has anticancer activity in PTEN-deficient glioblastoma and warrants further clinical study alone or in combination with PI3K pathway inhibitors.
|
18215105 |
2008 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Moreover, TRIM24 regulates the expression of DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) through PI3K/Akt/nuclear factor-κB signaling transduction and enhances resistance to temozolomide, the standard chemotherapeutic agent for glioblastoma.
|
24469053 |
2015 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
In addition, we demonstrate that the extracellular signal-regulated kinase (ERK)1/2 pathway is only partially implicated in the modulation of CXCL12-induced glioblastoma cell movement, whereas the phosphoinositol-3 kinase (PI3K) pathway is not involved.
|
20392929 |
2010 |