|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, effects of CDK4/6 inhibitors on various kinds of GBM cell lines are investigated and the functional mechanisms are identified.
|
31787897 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Design of a brain-penetrant CDK4/6 inhibitor for glioblastoma.
|
31307887 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
CDK4/6-dependent cell-cycle regulation is disrupted in most glioblastomas.
|
31285369 |
2019 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The purpose of this work is to elucidate the in vivo role of cytoplasmic Ccnd1-Cdk4 activity in the dissemination of GBM.
|
30957234 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conducted a phase Ib study (NCT02345824) to determine whether ribociclib, an inhibitor of cyclin-dependent kinases 4 and 6 (CDK4/6), penetrates tumor tissue and modulates downstream signaling pathways including retinoblastoma protein (Rb) in patients with recurrent glioblastoma (GBM).
|
31399936 |
2019 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Collectively, these findings demonstrate that the activation of c-Met/TrkA-B pathways is a novel mechanism involved in therapeutic resistance of GBM to CDK4/6 inhibition and that dual inhibition of c-Met/Trk with CDK4/6 should be considered in future clinical trials.<b>Significance:</b> CDK4/6 inhibition in glioblastoma activates the c-Met and TrkA-B pathways mediated by NF-κB and can be reversed by a dual c-Met/Trk inhibitor.<i></i>.
|
29844123 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the present study, we investigate efficacy of combination of palbociclib, cyclin-dependent kinase 4/6 (CDK4/6) inhibitor, and erlotinib, epidermal growth factor receptor (EGFR) inhibitor in GBM cell systems with different p53 status.
|
29508248 |
2018 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Characterization of diverse immune responses will facilitate patient stratification and improve personalized immunotherapy in the future.<b>Significance:</b> This study utilizes a computational approach to characterize the immune environments in glioblastoma and shows that glioblastoma immune microenvironments can be classified into three major subgroups, which are linked to typical glioblastoma alterations such as IDH mutation, NF1 inactivation, and CDK4-MARCH9 locus amplification.<b>Graphical Abstract:</b> http://cancerres.aacrjournals.org/content/canres/78/19/5574/F1.large.jpg <i></i>.
|
29921698 |
2018 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
LTS GB showed frequent chromosomal gains in 4q12 (platelet derived growth factor receptor alpha and KIT) and 12q14.1 (cyclin-dependent kinase 4), and deletion in 19q13.33 (BAX, branched chain amino-acid transaminase 2, and cluster of differentiation 33).
|
27932423 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further increasing the utility of the combination for brain cancers, everolimus significantly increases the brain concentration of palbociclib.<b>Conclusions:</b> Our findings demonstrate that the combination of CDK4/6 and mTOR inhibition has therapeutic potential against GBM and suggest it should be evaluated in a clinical trial.<i></i>.
|
28814434 |
2017 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Gene expression profiles of three glioma stem cell line samples, three normal astrocyte samples, three astrocyte overexpressing 4 iPSC-inducing and oncogenic factors (myc(T58A), OCT-4, p53DD, and H-Ras(G12V)) samples, three astrocyte overexpressing 7 iPSC-inducing and oncogenic factors (OCT4, H-Ras(G12V), myc(T58A), p53DD, cyclin D1, CDK4(RC24) and hTERT) samples and three glioblastoma cell line samples were downloaded from the ArrayExpress database (accession: E-MTAB-4771).
|
28952134 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
CDK4/6 inhibition is more active against the glioblastoma proneural subtype.
|
28903422 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Hence, our findings support that PIKE amplification or overexpression coordinately acts with CDK4 to drive GBM tumorigenesis.
|
28368413 |
2017 |
|
Glioblastoma
|
0.100 |
Biomarker
|
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 |
AlteredExpression
|
disease |
BEFREE |
Pharmacological inhibition or small interfering NTSR1 treatment blocked glioblastoma cell cycle progression in the G1 phase with a concomitantly decreased expression of CDK6, CDK4, and c-Myc.
|
26180082 |
2016 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Suppression of tumorigenicity by microRNA-138 through inhibition of EZH2-CDK4/6-pRb-E2F1 signal loop in glioblastoma multiforme.
|
23707559 |
2013 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings demonstrated for the first time that CDK4 was a downstream target of miR-124 and that CDA-2 could radiosensitize Glioblastoma multiforme cells through the MiR-124-CDK4 axis.
|
23761023 |
2013 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A recent study of CDK4/6 inhibitors in glioblastoma (GBM) xenografts identified retinoblastoma tumor suppressor protein RB1 status as a determinant of tumor therapeutic efficacy.
|
22157621 |
2012 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
p16-Cdk4-Rb axis controls sensitivity to a cyclin-dependent kinase inhibitor PD0332991 in glioblastoma xenograft cells.
|
22711607 |
2012 |
|
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Co-amplification of MDM2 and CDK4 that is present in 10% of glioblastomas was associated in most cases with deletion of the whole genomic region enclosed, including the WIF1 locus.
|
21642372 |
2011 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These results highlight the prognostic value of CDK4 amplification and of simultaneous EGFR-p53 alterations in the clinical outcome of patients with primary GBM.
|
19141386 |
2009 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
A search for loss of heterozygosity (LOH) on chromosome 1p, 9p, 10q, 19q, EGFR (epidermal growth factor receptor), CDK4, and MDM2 (mouse double minute) amplifications, CDKN2A (INK4A/ARF) homozygous deletions, p53 expression, was performed in a series of 220 primary glioblastomas.
|
16568472 |
2006 |
|
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Twelve glioblastomas (12%) showed amplification of PIKE with invariable co-amplification of the adjacent CDK4 gene.
|
16150119 |
2005 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We have studied gene amplification of genes located in 1q32 (GAC1, ELF3, MDM4, and ren1), 4q11 (PDGFR-alpha), and in 12q13-14 (MDM2 and CDK4) using quantitative real-time PCR in a group of 86 tumors consisting of 44 WHO grade IV glioblastomas (GBM) (34 primary and 10 secondary tumors), 21 WHO grade III anaplastic astrocytomas (AA), and 21 WHO grade II astrocytomas (AII).
|
16319692 |
2005 |
|
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Molecular genetic analysis of the TP53, PTEN, CDKN2A, EGFR, CDK4 and MDM2 tumour-associated genes in supratentorial primitive neuroectodermal tumours and glioblastomas of childhood.
|
12175345 |
2002 |