Glioblastoma Multiforme
|
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 Multiforme
|
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 Multiforme
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
To obtain a comprehensive view of these events, we leveraged the wide-spectrum GBM data available from The Cancer Genome Atlas project and performed an integrated analysis by systematically evaluating 9p21.3-related germline single-nucleotide polymorphisms, somatic copy number alterations (CNAs), DNA methylation, and microRNAs (miRNAs) with regard to CDKN2A/CDKN2B expression and patient prognosis in GBM.
|
21713760 |
2012 |
Glioblastoma Multiforme
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Results showed clear heterogeneity according to histologic subtypes of glioma, with TERT and RTEL variants a feature of astrocytic tumors and glioblastoma (GBM), CCDC26 and PHLDB1 variants a feature of astrocytic and oligodendroglial tumors, and CDKN2B variants most prominent in GBM.
|
21203894 |
2011 |
Glioblastoma Multiforme
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Homozygous deletion of the p16(INK4a)/p14(ARF)/p15(INK4b) locus is among the most common genetic alterations in GBM.
|
18974105 |
2008 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
On analysis of their respective recurrent tumors, five of six patients whose primary low-grade tumors carried p14(ARF) methylation exhibited homozygous co-deletions of the p14(ARF), p15(INK4b) and p16(INK4a) genes, which were restricted to glioblastoma as the most malignant end point.
|
17493032 |
2007 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Strong suppression of tumorigenicity was seen in four glioblastoma cell lines after transfection with p15 but not with p10.
|
11563632 |
2001 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Hypermethylation of N33, ER, HIC1, P16, P15 and c-abl were found in 61%, 59%, 60%, 5%, 2% and 0% of GBM respectively.
|
9671399 |
1998 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results indicate that loss of the p16 and p15 genes may be involved in tumor progression in human gliomas, especially in the development of glioblastoma, that this loss may give growth advantage to the cells in culture, and that it is not the result of culture artifacts.
|
7497469 |
1995 |
Glioblastoma Multiforme
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
No mutations were found in exon 2 of MTS2/p15 (12 cases examined), and one GBM showed a DNA deletion breakpoint in the 30 kb between MTS1/p16/CDKN2 and MTS2/p15 resulting in deletion of MTS1/p16/CDKN2 with retention of MTS2/p15.
|
7887443 |
1995 |
Glioblastoma Multiforme
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data suggest that the target of deletion in glioblastoma multiforme includes both p15 and p16 genes.
|
7987828 |
1994 |