|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
It was found that the AG and GG genotypes of the rs4977756 (CDKN2A/B) were associated with an increased risk of gliomas (OR 1.85 and OR 2.38) and glioblastomas (OR 2.77 and OR 3.94).
|
31721021 |
2020 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Four genes that were commonly altered in both primary and recurrent GBM were more prevalent in our cohort than reported in COSMIC: CDKN2A (86% vs. 53%) and CDKN2B (86% vs. 54%) deletions, EGFR activating mutation (52% vs. 10%) or amplification (81% vs. 45%), and TERT mutation (95% vs. 51%).
|
30535594 |
2019 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Nevertheless, specific mutations of p14ARF have been described in different types of human cancers such as colorectal and gastric carcinomas, melanoma and glioblastoma.
|
30836703 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we demonstrated that necrosis-inducing peptide P16 kills human glioblastoma cancer cells and primary human hepatoma or renal cancer cells isolated from patients who had not responded to standard treatments.
|
31206614 |
2019 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Because mutations of FANCA and BRAF and copy number variations of CDKN2A/B are more frequent in PXA than in glioblastoma, they might be used to distinguish the 2 tumors.
|
30496796 |
2019 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
BRAF V600E, TERT promoter mutations and CDKN2A/B homozygous deletions are frequent in epithelioid glioblastomas: a histological and molecular analysis focusing on intratumoral heterogeneity.
|
29105198 |
2018 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Here, we report a new subtyping method for GBM based on the genetic alterations of CDKN2A and TP53 genes.
|
29769617 |
2018 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
CDK4, CDK6, cyclin D1, p16(INK4a) and EGFR expression in glioblastoma with a primitive neuronal component.
|
29150788 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The p53-ARF-MDM2 pathway is deregulated in 84% of glioblastoma (GBM) patients and 94% of GBM cell lines.
|
30200436 |
2018 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Glioblastomas have a high frequency of mutations in the TERT promoter and CDKN2A locus that are expected to render them resistant to both replicative and oncogene-induced senescence.
|
28526854 |
2017 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
On real cancer data, pathTiMEx recapitulates previous knowledge on tumorigenesis, such as the temporal order among pathways which include APC, KRAS, and TP53 in colorectal cancer, while also proposing new biological hypotheses, such as the existence of a single early causal event consisting of the amplification of CDK4 and the deletion of CDKN2A in glioblastoma. pathTiMEx is available as an R package.
|
27936934 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we demonstrate that HBEGF can initiate GBM in mice in the context of Ink4a/Arf and Pten loss, and that these tumors are similar to the classical GBM subtype observed in patients.
|
28368403 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Additionally, GB presenting p53-negative staining associated with CDKN2A loss or p21 positivity represented a subtype with short survival.
|
26957305 |
2017 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Tumor types were characterized by specific broad and focal chromosomal events including focal loss of the INK4A/B locus in glioblastoma and loss of the RB1 gene and amplification of the PDGFRA gene in oligodendrogliomas.
|
27251041 |
2016 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Finally, five tumors were IDH wild-type (IDHwt) and had chromosome seven gains, chromosome 10 losses, and homozygous 9p deletions (CDKN2A), alterations typical of IDHwt (primary) GBM.
|
26757882 |
2016 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Deletion of CDKN2A and CDKN2B loci was found both in diffuse astrocytoma and glioblastoma component, but no other significant alterations were found.
|
26404554 |
2016 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the RCAS/Ntv-a glia-specific transgenic mouse model, c-Myc increased the GBM incidence from 19.1% to 47.4% by 12 weeks of age when combined with kRas and Akt3 in Ntv-a INK4a-ARF (also known as CDKN2A)-null mice.
|
26993778 |
2016 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
CD47 activation-induced UHRF1 over-expression is associated with silencing of tumor suppressor gene p16INK4A in glioblastoma cells.
|
25550546 |
2015 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The tumoricidal and TMZ-sensitizing effects of BI2536 were uniformly observed across Ink4a/Arf(-/-) EGFRvIII glioblastoma clones that acquired independent resistance mechanisms to EGFR inhibitors, suggesting these resistant clones retain oncogenic stress that required PLK1 compensation.
|
26059434 |
2015 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Intriguingly, our data also suggest that nearly half of GB cell lines have a combination of TP53 mutation and CDKN2A homozygous deletion, which are considered as mutually exclusive in glioblastoma.
|
24498027 |
2014 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Copy number changes in chromosomes 1p and 19q were associated with GII/IIIs, while these changes in CDKN2A, PTEN and EGFR were more commonly associated with GBMs.
|
24614622 |
2014 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Elacridar also markedly improved TMZ/ABT-888 combination treatment in the spontaneous p53;p16(Ink4a)/p19(Arf);K-Ras(v12);LucR glioblastoma model.
|
24647572 |
2014 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we report that loss of tumor suppressor P14ARF can contribute to activating the clotting cascade in glioblastoma.
|
24398474 |
2014 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Finally, the G-CIMP+ Ink4a-Arf-/- EGFRvIII glioblastoma line was more resistant to the EGFR inhibitor, Gefitinib, relative to its isogenic G-CIMP- counterpart.
|
25277177 |
2014 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
CDKN2A deletion was noted in 40.3% cases of GBM with majority being homozygous deletion (74%).
|
23311918 |
2013 |