Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Additionally, DHX33 was found to be induced by inhibitors of PI3K and mTOR whose activation has been detected in 50% of glioblastoma.
|
30552990 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The Oncogene Addiction Switch from NOTCH to PI3K Requires Simultaneous Targeting of NOTCH and PI3K Pathway Inhibition in Glioblastoma.
|
30669546 |
2019 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Carnosine inhibits glioblastoma growth independent from PI3K/Akt/mTOR signaling.
|
31247000 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, the combined inhibition of PI3K/Akt/mTOR and SHH pathways was superior to single pathway inhibition in suppressing glioblastoma growth by targeting GICs.
|
30251117 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings thus provide rational evidence that the combination of Pt3glc with PI3K inhibitor, which target alternative pathways in GBM cells, may be a useful adjuvant therapy in glioblastoma treatment.
|
29336479 |
2019 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
SIGNIFICANCE: These findings provide novel insights into the mechanisms of PI3K inhibitor resistance in glioblastoma.
|
31416846 |
2019 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overexpression of HOXC10 promotes glioblastoma cell progression to a poor prognosis via the PI3K/AKT signalling pathway.
|
29768063 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overall, our findings propose that miR-579 functions as a novel tumor suppressor gene in GBM by regulating the PI3K/AKT signaling pathway and may serve as a therapeutic target for clinical therapy of glioblastoma multiform.
|
31243804 |
2019 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This study was a multicenter, open-label, multi-arm, phase II trial in patients with PI3K pathway-activated glioblastoma at first or second recurrence.
|
30715997 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PIP4K2A as a negative regulator of PI3K in PTEN<i>-</i>deficient glioblastoma.
|
30898893 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Serum‑derived hepatitis C virus can infect human glioblastoma cell line SF268 and activate the PI3K‑Akt pathway.
|
30896873 |
2019 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Up-regulated circular RNA hsa_circ_0067934 contributes to glioblastoma progression through activating PI3K-AKT pathway.
|
31081099 |
2019 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
At last, rescue assays validated that PI3K/Akt/mTOR signaling pathway involved in the glioblastoma progression mediated by SNHG20.
|
30943748 |
2019 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Genetic lesions in glioblastoma (GB) include constitutive activation of PI3K and EGFR pathways to drive cellular proliferation and tumor malignancy.
|
30506943 |
2019 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
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 |
Childhood Glioblastoma
|
0.100 |
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 |