|
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 |
GeneticVariation
|
disease |
BEFREE |
(1) Amplification of EGFR was observed in well-characterised TNBCs (up to 92%); (2) qPCR correlated with SISH with 94% specificity and 75.6% sensitivity; (3) IHC correlated with SISH with 97% sensitivity and 78% specificity; (4) no EGFR, Kras mutations or EML4-ALK translocations were found, but PI3K and Braf mutations were observed in 26% of cases; and (5) small, acentric circular extrachromosomal DNA similar to 'double minutes' in glioblastomas was observed in 18% of SISH sections.
|
24423920 |
2014 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
2-(2-(2,4-dioxopentan-3-ylidene)hydrazineyl)benzonitrile as novel inhibitor of receptor tyrosine kinase and PI3K/AKT/mTOR signaling pathway in glioblastoma.
|
30731398 |
2019 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Glioblastomas frequently carry genetic alterations resulting in an aberrant activation of the phosphoinositol-3-kinase (Pi3k)/protein kinase B (Akt) signalling pathway, including most notably phosphatase and tensin homolog (PTEN) mutation, epidermal growth factor receptor (EGFR) amplification and rearrangement, as well as carboxyl-terminal modulator protein (CTMP) hypermethylation [Knobbe et al., (2004) Hypermethylation and transcriptional downregulation of the carboxyl-terminal modulator protein gene in glioblastomas.J Natl Cancer Institute, 96, 483-486].
|
16150119 |
2005 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Glioblastoma (GBM) genomes feature recurrent genetic alterations that dysregulate core intracellular signaling pathways, including the G1/S cell cycle checkpoint and the MAPK and PI3K effector arms of receptor tyrosine kinase (RTK) signaling.
|
23814263 |
2013 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
PI3K-AKT pathway negatively controls EGFR-dependent DNA-binding activity of Stat3 in glioblastoma multiforme cells.
|
16007122 |
2005 |
|
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 |
PI3K/Akt, Sonic Hedgehog (SHH), and PKA pathways play major regulatory roles in the progression of GBM.
|
30669581 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Aberrations of the RTK/RAS/PI3K-, p53-, and RB cell signaling pathways were recognized as a core requirement for pathogenesis of glioblastoma.
|
23536279 |
2013 |
|
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 |
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 |
Animal studies have shown cooperative contribution of the Ras/Raf/MAPK and PI3K/Akt/mTOR signaling pathways in glioblastoma formation.
|
24048798 |
2011 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Anti-neoplastic activity of low-dose endothelial-monocyte activating polypeptide-II results from defective autophagy and G2/M arrest mediated by PI3K/Akt/FoxO1 axis in human glioblastoma stem cells.
|
24792437 |
2014 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Application of a specific extracellular-related kinase 1/2 (ERK1/2) inhibitor, but not application of either an protein kinase B (Akt) inhibitor, or a Jun N-terminal kinase (JNK) inhibitor to VEGFa-overexpressing A-172 cells substantially abolished the effect of VEGFa on MMP2 activation, suggesting that VEGFa may increase MMP2 levels via ERK/mitogen-activated protein kinase (MAPK), but not phosphatidylinositol 3-kinase (PI3K) or JNK signaling pathways in glioblastoma.
|
25213694 |
2014 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Applied to data from the Cancer Genome Atlas (TCGA), the method identifies the principal known altered modules in glioblastoma (GBM) and highlights the striking mutual exclusivity of genomic alterations in the PI(3)K, p53, and Rb pathways.
|
21908773 |
2012 |
|
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 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Both mitogen-activated protein kinase (MAPK)/extracellular-signal-regulated kinases (ERK) 1/2 and phosphatidylinositide-3-OH kinase (PI3K)/Akt pathways regulate activation of E-twenty-six (ETS)-like transcription factor 1 (Elk-1) in U138 glioblastoma cells.
|
22085529 |
2012 |
|
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 |
By identifying class I PI3K inhibitors as powerful agents in enhancing the lethality of DNA-damaging drugs, to which GBMs are usually considered unresponsive, our findings have important implications for the design of rational combination regimens in overcoming the frequent chemoresistance of GBM.
|
19633683 |
2009 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Carnosine inhibits glioblastoma growth independent from PI3K/Akt/mTOR signaling.
|
31247000 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
CD133 and DNA-PK regulate MDR1 via the PI3K- or Akt-NF-κB pathway in multidrug-resistant glioblastoma cells in vitro.
|
25823028 |
2016 |
|
Glioblastoma
|
0.100 |
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 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Collectively, these results indicate that GA-A may encourage U251 cell growth and invasion/migration inhibition, apoptosis, and autophagy through the inactivation of PI3K/AKT signaling pathway in human GBM.
|
31503386 |
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 |
Biomarker
|
disease |
BEFREE |
Correction: Opposing Effects of PI3K/Akt and Smad-Dependent Signaling Pathways in NAG-1-Induced Glioblastoma Cell Apoptosis.
|
30281640 |
2018 |