Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
MiR-223/PAX6 Axis Regulates Glioblastoma Stem Cell Proliferation and the Chemo Resistance to TMZ via Regulating PI3K/Akt Pathway.
|
28332226 |
2017 |
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Recent advances in the use of PI3K inhibitors for glioblastoma multiforme: current preclinical and clinical development.
|
28592260 |
2017 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Compared with the GBM NG2- cells from the same tumor, the GBM of NG2+ cells overexpress genes associated with aggressive tumorigenicity, including overexpression of Mitosis and Cell Cycling Module genes (e.g., MELK, CDC, MCM, E2F), which have been previously shown to correlate with poor survival in GBM.
|
21798846 |
2011 |
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
However, due to the development of resistance mechanisms, kinase inhibition studies targeting the PI3K-AKT pathway for relapsing glioblastoma have mostly failed thus far.
|
25256166 |
2014 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
In the present study, we report decreased cell proliferation and invasive ability upon the LY294002-induced inhibition of PI3K in both U251 and LN229 human glioblastoma cells in vitro.
|
20888802 |
2010 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Multiple lesions in the receptor tyrosine kinases (RTKs) pathway including PTEN mutation, co-activation of RTKs, and EGFRvIII mutation resulted in unaltered active status of PI3K/mTOR in the GBM lines even in the presence of EGFR inhibition.
|
24658109 |
2014 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
These results suggest that genetic alterations of class IA PI3K subunit genes can occasionally play a role in human glioblastoma by activating the PI3K-AKT signaling pathway independently of PTEN mutation.
|
15605984 |
2004 |
Glioblastoma Multiforme
|
0.500 |
AlteredExpression
|
disease |
BEFREE |
We previously reported that decreased miR-218 expression in GBM directly promotes RTK activity by increasing the expression of key RTKs and their signaling mediators, including the RTK epidermal growth factor receptor (EGFR), phospholipase C-γ1 (PLCγ1), and the kinases PIK3CA and ARAF.
|
25943352 |
2015 |
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Recurrent PIK3CA missense mutations (PIK3CAmut) in GBM are restricted to three functional domains: adaptor binding (ABD), helical, and kinase.
|
29975751 |
2018 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Correction: Opposing Effects of PI3K/Akt and Smad-Dependent Signaling Pathways in NAG-1-Induced Glioblastoma Cell Apoptosis.
|
30281640 |
2018 |
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Gene expression and clinical relevance of PI3K genes in GBM patients were analyzed using online databases.
|
29016844 |
2018 |
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
In this study, we determined the effect of anti-GRP78 antibody and the combined effect of the anti-GRP78 antibody with ionizing radiation (XRT) on NSCLC and GBM cell lines both <i>in vitro</i> and <i>in vivo</i><b>Experimental Design:</b> NSCLC and GBM cancer cell lines were treated with anti-GRP78 antibodies and evaluated for proliferation, colony formation, cell death, and PI3K/Akt/mTOR signaling.
|
27815359 |
2017 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Downregulation of uPA inhibits migration and PI3k/Akt signaling in glioblastoma cells.
|
12545160 |
2003 |
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
CausalMutation
|
disease |
CGI |
|
|
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Our results uncover CD95 as an activator of PI3K and, most importantly, as a crucial trigger of basal invasion of glioblastoma in vivo.
|
18328427 |
2008 |
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
The suggested dependence of glioblastoma tumors on PI3K signaling implies that PI3K inhibitors should lead to effective killing of these cancer cells, but that has been shown not to be the case.
|
19076776 |
2009 |
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 |