|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Briefly, LOC441204 bound to β-catenin preventing its degradation, resulting in downstream p21 repression and cdk4 activation to enhance glioma cell proliferation.
|
28717243 |
2017 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
More importantly, TMEM45A siRNA treatment significantly down-regulated the proteins promoting cell cycles transition (Cyclin D1, CDK4 and PCNA) and cell invasion (MMP-2 and MMP-9), which indicted a possible mechanism underlying its functions on glioma.
|
26722455 |
2015 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we demonstrated that elevated CDK4 expression is correlated with poor prognosis in glioma after radiotherapy and that CDK4 knockdown conferred radiosensitivity in glioma cell lines.
|
23761023 |
2013 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
MDM2, MDM4, CDK4 and PIK3C2B are known for potentially being amplified or overexpressed in high-grade gliomas.
|
22825724 |
2012 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This paper elucidates a model to regulate glioma cell cycle progression in which hUCBSC acts to control cyclin D1 induction and in concert its partner kinases, Cdk 4 and Cdk 6 by mediating cell cycle arrest at G(0)-G(1) phase.
|
21455311 |
2011 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, whereas germ-line mutations of PTEN, p53, p16(INK4A)/p14(ARF), and CDK4 are not common events in familial glioma, outside of familial cancer syndromes, point mutations of p53 and hemizygous deletions and other rearrangements of the p16(INK4A)/p14(ARF) tumor suppressor region may account for a subset of familial glioma cases.
|
10797439 |
2000 |
|
Glioma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Thus, despite the association between the sporadic forms of high-grade glioma and abnormalities of p16(INK4A), p15(INK4B), or CDK4, we found no evidence that germ-line mutations in the coding region of these three genes predispose to inherited glial tumors.
|
9815774 |
1997 |
|
Glioma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Alterations in P16ink4 or in the gene encoding one of its ligands, cyclin-dependent kinase 4 (CDK4), have been reported in human glioma cell lines and primary tumors but not in primitive neuroectodermal tumors (PNETs), the most common malignant brain tumor of childhood.
|
8847566 |
1996 |
|
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
All the glioma cell lines expressed similar levels of the retinoblastoma protein and no amplification of the cyclin-dependent kinase 4 gene.
|
8649864 |
1996 |
|
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Lack of p16INK4 or retinoblastoma protein (pRb), or amplification-associated overexpression of cdk4 is observed in distinct subsets of malignant glial tumors and cell lines.
|
7585516 |
1995 |
|
Glioma
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Homozygous deletion of the MTS1/p16 and MTS2/p15 genes and amplification of the CDK4 gene in glioma.
|
7478535 |
1995 |
|
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These results suggest: (a) the involvement of P16INK4 in glioma progression; (b) that mechanisms other than mutation or deletion can down-regulate expression of the p16/CDKN2 gene; and (c) that the balance between CDK4 and its cognate inhibitor, P16INK4, may confer a cell growth advantage and facilitate tumor progression.
|
7728764 |
1995 |
|
Glioma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here we have examined 32 glioma cell lines for amplification-associated overexpression of the CDK4 gene as an alternative mechanism for abrogating the growth-regulatory effects of p16.
|
7954404 |
1994 |