Meningioma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Notch and PI3K/AKT/mTOR) differences between convexity and skull base meningiomas.
|
31077268 |
2019 |
Meningioma
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
Genetic aberrations (TRAF7, KLF4, AKT1, and SMO) and the effects of genetic aberrations on the expression of inhibitory immune checkpoint molecules (PD-L1, IDO, and TDO2) in skull base meningiomas are still unclear.
|
31177425 |
2019 |
Meningioma
|
0.700 |
Biomarker
|
disease |
BEFREE |
However, several clinical trials are under way evaluating the efficacy of chemotherapies, such as trabectedin, and novel molecular agents targeting Smoothened, AKT1, and focal adhesion kinase in patients with recurrent meningiomas.
|
30649489 |
2019 |
Meningioma
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
Meningiomas frequently display activation of the PI3K/AKT/mTOR pathway, leading to elevated levels of phospho-eukaryotic translation initiation factor 4E binding proteins, which enhances protein synthesis; however, it is not known whether inhibition of protein translation is an effective treatment option for meningiomas.
|
28610844 |
2018 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
The importance of NF2 (neurofibromin 2), TRAF7 (tumor necrosis factor [TNF] receptor-associated factor 7), KLF4 (Kruppel-like factor 4), AKT1, SMO (smoothened), PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha), and POLR2 (RNA polymerase II subunit A) demonstrates that there are at least 6 distinct mutational classes of meningiomas.
|
29852774 |
2018 |
Meningioma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Furthermore, the functional consequences of introducing an AKT inhibitor in OGN-overexpressing meningioma cells were assessed.
|
28923059 |
2017 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
This is the first report of an AKT1-mutant meningioma responding to AKT inhibition, suggesting that molecular screening may result in clinical benefit.
|
28376212 |
2017 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Meningiomas in the SMO-mutant group had an overall 36% recurrence rate, significantly higher than in the AKT1-mutant group (16%) and in the "SMO and AKT1 wildtype" group (11%) (χ2 test, P = .04).
|
28082415 |
2017 |
Meningioma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Genotyping of SMO and AKT1 is likely to be high yield in anterior skull base meningiomas with available surgical tissue.
|
27885953 |
2017 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
We analyzed 93 skull base meningiomas (82 WHO grade I, 11 WHO grade II) for mutations of hot spots or the most relevant exons of AKT1, KLF4/TRAF7, SMO, PI3K, and the TERT promoter.
|
28482067 |
2017 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Cranial hyperostosis and meningiomas are common in patients with Proteus syndrome, which is caused by a somatic activating mutation in AKT1 c.49G>A.
|
27550858 |
2016 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
We used high-resolution array-comparative genomic hybridization to prospectively characterize copy-number changes in 150 meningiomas and then characterized these samples for mutations in AKT1, KLF4, NF2, PIK3CA, SMO, and TRAF7.
|
26826201 |
2016 |
Meningioma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Furthermore, PI3K/AKT may contribute to the carcinogenesis and development of human meningiomas in combination with HER-2.
|
25998419 |
2015 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Thus, monosomy 22, which is often associated with mutations of the NF2 gene, has emerged as the most frequent alteration of meningiomas; in addition, several other genes (e.g., AKT1, KLF4, TRAF7, SMO) and chromosomes have been found to be recurrently altered often in association with more complex karyotypes and involvement of multiple signaling pathways.
|
25965831 |
2015 |
Meningioma
|
0.700 |
Biomarker
|
disease |
BEFREE |
The recent identification of somatic mutations in components of the SHH-GLI1 and AKT1-MTOR signaling pathways indicates the potential for cross talk of these pathways in the development of meningiomas.
|
25857641 |
2015 |
Meningioma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Inhibition of TGM2 function by siRNA or cystamine induced meningioma cell death, which was associated with reduced AKT phosphorylation and caspase-3 activation.
|
25247996 |
2014 |
Meningioma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
A subset of meningiomas lacking NF2 alterations harbored recurrent oncogenic mutations in AKT1 (p.Glu17Lys) and SMO (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways.
|
23334667 |
2013 |
Meningioma
|
0.700 |
Biomarker
|
disease |
CTD_human |
A subset of meningiomas lacking NF2 alterations harbored recurrent oncogenic mutations in AKT1 (p.Glu17Lys) and SMO (p.Trp535Leu) and exhibited immunohistochemical evidence of activation of these pathways.
|
23334667 |
2013 |
Meningioma
|
0.700 |
Biomarker
|
disease |
HPO |
|
|
|
Meningioma
|
0.700 |
CausalMutation
|
disease |
CGI |
|
|
|