|
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 |
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 |
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
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Although these results need to be confirmed in larger series as well as under different treatment conditions, our retrospective study shows clear evidence that p15 methylation is an important prognostic factor for survival and underlines that this tumor suppressor, involved in cell cycle control, is an attractive candidate for therapeutic approaches in glioblastomas.
|
19424593 |
2009 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Conspirators in a capital crime: co-deletion of p18INK4c and p16INK4a/p14ARF/p15INK4b in glioblastoma multiforme.
|
18974105 |
2008 |
|
Glioblastoma
|
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
|
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
The genes encoding the cyclin-dependent kinase inhibitors p16INK4A (CDKN2A) and p15INK4B (CDKN2B) are frequently homozygously deleted in a variety of tumor cell lines and primary tumors, including glioblastomas in which 40-50% of primary tumors display homozygous deletions of these two loci.
|
10939591 |
2000 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Sixty-seven percent of GBs (91/136) and 21% of AAs (8/39) had abnormalities of the G1-S control system either by mutation/homozygous deletion of RB1, CDKN2A or CDKN2B, or amplification of CDK4.
|
10667596 |
2000 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In contrast, 7/13 glioblastomas with hemizygous deletions of CDKN2A and 8/11 glioblastomas with hemizygous deletions of CDKN2B showed no or weak expression.
|
9000591 |
1997 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
As a whole, the data assign a tumor suppressor role to p15 and confirm homozygous deletions as the favorite mechanism for the inactivation of MTS1 and MTS2 in glioblastomas.
|
8526910 |
1995 |
|
Glioblastoma
|
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data suggest that the target of deletion in glioblastoma multiforme includes both p15 and p16 genes.
|
7987828 |
1994 |