|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Given this disparity and to address the relation of patient age to mutation frequency, we examined 10 exons of PIK3CA in 73 glioblastoma samples by PCR amplification followed by direct DNA sequencing.
|
17050665 |
2006 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The objective of this study was to examine whether PIK3CA mutations are associated with a specific clinical phenotype in glioblastoma.
|
31036078 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Only one glioblastoma showed both PIK3CA mutation and amplification.
|
17235514 |
2007 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Introduction of normal PTEN together with H-Ras(G12V) into U251 glioblastoma cells reduced the PI3K-dependent activation of Akt, but had no effect on vacuolation.
|
17210246 |
2007 |
|
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
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 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 |
GeneticVariation
|
disease |
BEFREE |
In this study, we performed a synthetic lethality screen to identify genes or pathways whose inactivation, in combination with the PI3K inhibitors PX-866 and NVPBEZ-235, might result in a lethal phenotype in glioblastoma multiforme (GBM) cells.
|
21430111 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Typical molecular changes in glioblastoma include mutations in genes regulating receptor tyrosine kinase (RTK)/rat sarcoma (RAS)/phosphoinositide 3-kinase (PI3K), p53, and retinoblastoma protein (RB) signaling.
|
26948367 |
2016 |
|
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
PIK3CA mutations in glioblastoma multiforme.
|
15924253 |
2005 |
|
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Our findings are the first to suggest that within a glioblastoma tumour the PI3K network can have distinct, cell-specific functions.
|
29184057 |
2017 |
|
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
For example, combining gefitinib with inhibitors of the PI3K/AKT pathway show enhanced cytotoxicity in glioblastoma derived cell lines.
|
18566746 |
2008 |
|
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
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 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Epidermal growth factor receptor (EGFR) mutations (EGFRvIII) and phosphoinositide 3-kinase (PI3K) hyperactivation are common in GBM, promoting tumor growth and survival, including through sterol regulatory element-binding protein 1 (SREBP-1)-dependent lipogenesis.
|
22059152 |
2011 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Our study demonstrates, for the first time, that vaults have a tumour-promoting potential by stabilizing EGFR/PI3K-mediated migration and survival pathways in human glioblastoma.
|
24243798 |
2013 |
|
Glioblastoma Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Mechanistically, cPLA2α knockdown significantly suppresses the PI3K/Akt/mTOR pathway in glioblastoma cells.
|
30360807 |
2018 |
|
Glioblastoma Multiforme
|
0.500 |
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 Multiforme
|
0.500 |
Biomarker
|
disease |
BEFREE |
Nevertheless, the administration of the dual PI3K/mTOR inhibitor BEZ235 potentiated the effect of TMZ plus MET on cell viability, inducing a pro-apoptotic phenotype during hypoxic condition also in T98 cells, suggesting the block of the PI3K/AKT/mTOR pathway as a complementary target to further overcome GBM resistance during hypoxia.
|
31214505 |
2019 |
|
Glioblastoma Multiforme
|
0.500 |
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 |