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 |
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 |
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 |
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 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Purpose:</b> In this study, we took efforts to assess the effects of PI3K/mTOR blockade by XL765 on GBM growth <i>in vitro</i> and <i>in vivo</i>.
|
31360067 |
2019 |
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 |
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 |
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 |
Glioblastoma
|
0.100 |
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
|
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 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The 2-DG induced suppression of miR-7-5p in turn activated the PI3K/Akt signaling activator Trefoil Factor 3 (TFF3) in GBM cell lines.
|
29621542 |
2018 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The Cancer Genome Atlas integrative analysis of GBM reported the striking finding of genetic alterations in the p53 and PI3K pathways in more than 80% of GBMs.
|
28838997 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therapies targeting the PI3K/AKT/Afadin pathway may therefore be beneficial for reducing the angiogenic potential of glioblastoma.
|
29434887 |
2018 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
TERT promoter wild-type glioblastomas show distinct clinical features and frequent PI3K pathway mutations.
|
30333046 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overall, the data suggests the existence of intratumor subtype heterogeneity in GBM and that using combinations of both MAPK and PI3K drug inhibitors is necessary for effective targeted therapy.
|
29852183 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Correction: Opposing Effects of PI3K/Akt and Smad-Dependent Signaling Pathways in NAG-1-Induced Glioblastoma Cell Apoptosis.
|
30281640 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Mechanistically, cPLA2α knockdown significantly suppresses the PI3K/Akt/mTOR pathway in glioblastoma cells.
|
30360807 |
2018 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Both pathways are also activated in GBM cell lines, however, only the PI3K pathway seems to play a crucial role in resistance to alkylating agents and might serve as drug target for chemosensitization.
|
29755294 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta (PIK3CB)/p110β (a PI3K catalytic isoform) by RNAi substantially suppresses GBM growth with less toxicity to normal astrocytes.
|
30312846 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
PI3K and MAPK inhibitors have been studied preclinically in GBM as monotherapy, but not in combination with radiotherapy, which is a key component of the current standard treatment of GBM.
|
28958992 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Gene expression and clinical relevance of PI3K genes in GBM patients were analyzed using online databases.
|
29016844 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, the differential expression of the immunomodulatory molecule YKL-40 may affect the treatment efficacy of PI3K/AKT-based pathway inhibitors in glioblastoma.
|
29729901 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here we identified that WEE1 is activated after transient exposure to PI3K inhibition and confers resistance to PI3K inhibition in GBM.
|
29016926 |
2018 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this review, we clarify the importance of 4EBP1 as a biomarker for the efficacy of PI3K-AKT-mTOR inhibitors in glioblastoma.
|
28696243 |
2018 |
Glioblastoma
|
0.100 |
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 |