Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
LncRNA-XIST functioned as a competing endogenous RNA of miR-126 and then regulated IRS1/PI3K/Akt pathway in glioblastoma cells.
|
31680298 |
2020 |
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 |
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 |
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 |
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 |
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 |
Therefore, while under normoxic conditions, EGF stimulates the activation of both the PI3K and the MAPK pathways and the induction of VEGF, in glioblastoma cells, hypoxic conditions lead to the suppression of the PI3K/RhoA/C pathway and an exclusive switch to the MAPK pathway.
|
31698752 |
2019 |
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Notch activity in GBM was also shown to be associated with hypoxia and certain cancer-related molecular pathways such as PI3K/AKT/mTOR and ERK/MAPK.
|
31376551 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The PI3K/AKT/mTOR pathway activation plays a central role in glioblastoma multiforme (GBM) development and progression, and in resistance to anti-cancer therapies.
|
31707687 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Tivantinib (1 μmol/L) in combination with PI3K inhibitor LY294002 (0.5 μmol/L) and mTOR inhibitor rapamycin (0.1 nmol/L) largely inhibited the proliferation of glioblastoma cells.
|
31575848 |
2019 |
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Genomic analyses reveal that signature genetic lesions in GBM and LGG include copy gain and amplification of chromosome 7, amplification, mutation, and overexpression of receptor tyrosine kinases (RTK) such as EGFR, and activating mutations in components of the PI3K pathway.
|
30530503 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
SIGNIFICANCE: These findings provide novel insights into the mechanisms of PI3K inhibitor resistance in glioblastoma.
|
31416846 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Serum‑derived hepatitis C virus can infect human glioblastoma cell line SF268 and activate the PI3K‑Akt pathway.
|
30896873 |
2019 |
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
Here we show that overexpression of NEU3 in glioblastoma U87MG cells activates PI3K/Akt signaling pathway resulting in an increased radioresistance capacity and in an improved efficiency of double strand DNA-repair mechanisms after irradiation.
|
30466783 |
2019 |
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
GDC-0084 is a brain penetrant, dual PI3K/mTOR inhibitor that has shown promising activity in a preclinical model of glioblastoma.
|
30796030 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The Oncogene Addiction Switch from NOTCH to PI3K Requires Simultaneous Targeting of NOTCH and PI3K Pathway Inhibition in Glioblastoma.
|
30669546 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
These results demonstrated that miR-605 acts as a tumor suppressor in the development of GBM by directly targeting SOX9 and inhibiting the activation of the PI3K/Akt pathway, suggesting its potential role as a therapeutic target for GBM.
|
31360068 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
At last, rescue assays validated that PI3K/Akt/mTOR signaling pathway involved in the glioblastoma progression mediated by SNHG20.
|
30943748 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Mutations in TERT, CDKN2A/CDKN2B, EGFR, and PI3K pathway were commonly observed in both primary and recurrent GBM revealing their prognostic and therapeutic potential.
|
30535594 |
2019 |
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, DPT effectively inhibited the expression of PI3K and downregulated PI3K/Akt‑mediated signaling pathways to prevent glioblastoma progression.
|
30816477 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Molecular genetic aberrations in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway are common in human cancers including glioblastoma, yet, novel therapeutic approaches targeting this pathway in glioblastoma have not been successful.
|
31618458 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
PIP4K2A as a negative regulator of PI3K in PTEN<i>-</i>deficient glioblastoma.
|
30898893 |
2019 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Chen and colleagues leverage a <i>Drosophila</i> GBM model to identify a conserved signaling axis downstream of the EGFR and PI3K that involves the death-associated protein kinase (Drak), a cytoplasmic serine/threonine kinase orthologous to the human kinase STK17A.
|
30877099 |
2019 |