|
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 |
GeneticVariation
|
disease |
BEFREE |
Recently, a large-scale mutational analysis of eight PI3K and eight PI3K-like genes revealed somatic mutations in PIK3CA, which encodes the p110alpha catalytic subunit of class IA PI3K, in several types of cancer, including glioblastoma multiforme.
|
17050665 |
2006 |
|
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 |
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
|
0.100 |
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
|
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 |
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 |
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
|
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 |
Here, we report on the analysis of 17 genes related to the Pi3k/Akt signalling pathway for genetic alteration and aberrant expression in a series of 103 glioblastomas.
|
14655756 |
2003 |
|
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |