|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Genetic analyses demonstrated that EGFR-Ras and PI3K induce fly glial neoplasia through activation of a combinatorial genetic network composed, in part, of other genetic pathways also commonly mutated in human glioblastomas.
|
21538561 |
2011 |
|
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 |
Biomarker
|
disease |
BEFREE |
We synthesized Gint4.T-conjugated PNPs able of high uptake into U87MG glioblastoma (GBM) cells and with astonishing EC<sub>50</sub> value (38 pM) when loaded with a PI3K-mTOR inhibitor.
|
28471660 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
FoxO proteins or loss of functional p53 maintain stemness of glioblastoma stem cells and survival after ionizing radiation plus PI3K/mTOR inhibition.
|
27448972 |
2016 |
|
Glioblastoma
|
0.100 |
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
|
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 |
|
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 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, there is reason for renewed optimism given the now very detailed knowledge of the cancer genome in GBM and a wealth of novel compounds entering the clinic, including next generation RTK inhibitors, class I PI3K inhibitors, mTOR kinase inhibitors (TORKinibs), and dual PI3(K)/mTOR inhibitors.
|
22015553 |
2012 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Mutation or deletion of PTEN has been found in as high as 80% of glioblastomas, which harbor aberrant cell signaling passing through the phosphatidylinositol-3-kinase (PI3K) and Akt (PI3K/Akt) survival pathway.
|
17616812 |
2007 |
|
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 |
Our objectives were to test a dual PI3K/mTOR inhibitor that may cross the blood-brain barrier (BBB) and provide the rationale for using this inhibitor in combination regimens to chemotherapy-induced synergism in GBM.
|
28423515 |
2017 |
|
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 |
Further, photofrin based PDT followed by miR-99a transfection dramatically increased miR-99a expression and also increased apoptosis in glioblastoma cell cultures and drastically reduced tumor growth in athymic nude mice, due to down regulation of fibroblast growth factor receptor 3 (FGFR3) and PI3K/Akt signaling mechanisms leading to inhibition of cell proliferation and induction of molecular mechanisms of apoptosis.
|
23409016 |
2013 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest that there is p70S6K-mediated, cross-inhibitory regulation between the MEK/ERK and PI3K/mTOR pathways, in which each contribute to the maintenance of the self-renewal and tumorigenic capacity of glioblastoma CSLCs.
|
20857497 |
2010 |
|
Glioblastoma
|
0.100 |
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
Overexpression of HOXC10 promotes glioblastoma cell progression to a poor prognosis via the PI3K/AKT signalling pathway.
|
29768063 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Up-regulated circular RNA hsa_circ_0067934 contributes to glioblastoma progression through activating PI3K-AKT pathway.
|
31081099 |
2019 |
|
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 |
Our results show that our in vitro NMR-detected changes in lactate and choline metabolites may have potential as non-invasive biomarkers for monitoring response to combination of PI3K/mTOR inhibitors with TMZ during clinical trials in children with glioblastoma, subject to further in vivo validation.
|
28704425 |
2017 |
|
Glioblastoma
|
0.100 |
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
|
0.100 |
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
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway is over-activated in glioblastoma and has been revealed to be potentially implicated in resistance to TMZ.
|
29151909 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
CsA, comparably to pharmacological inhibitors of PI3K/Akt signaling (LY294002, A443654), reduced motility of glioblastoma cells, diminished MMP-2 gelatinolytic activity and MMP-2 and MT1-MMP expression.
|
21276823 |
2011 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, we detected decreased nuclear localization of Nrf2 following combined treatment with ERK and PI3K inhibitors in three human glioblastoma cell lines and selected the cell line (U251) most sensitive to the inhibitors for further study.
|
23708697 |
2013 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Primate-specific miR-663 functions as a tumor suppressor by targeting PIK3CD and predicts the prognosis of human glioblastoma.
|
24523440 |
2014 |