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 |
The aim of the present study was to analyze the frequency of CDKN2A gene deletions in GBM and correlate CDKN2A deletional status with (i) age of the patient (ii) p16 protein expression and (iii) other genetic alterations, namely EGFR amplification and TP53 mutation.
|
23311918 |
2013 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Immunohistochemial p16 loss was more frequent in pGBs, whereas p53, epidermal growth factor receptor, and phosphatase and tensin homolog loss were similar to that of aGBs.
|
22570167 |
2012 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We treated human glioblastoma cells with BP and found a dose-dependent decrease in human telomerase reverse transcriptase (hTERT) mRNA expression and a concomitant increase in p16 and p21 expression.
|
21553143 |
2011 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Differential expression of microenvironment genes and p16 locus deletion are associated with responses to radiation therapy and to first-line chemotherapy, respectively, in GBM.
|
20822523 |
2010 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Additionally, the combination of p16 and p21(CIP1) (p21-S154A) peptides dramatically suppressed the growth of glioblastoma line Gli36DeltaEGFR, which carries a missense mutation in p53, by >97% after 120 h. Significantly, our murine brain tumor model for dual-peptide delivery showed a substantial average survival enhancement (P < 0.0001) for peptide-treated mice.
|
18566217 |
2008 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The U251 glioblastoma and a glioblastoma xenograft cell line transduced with a recombinant replication-defective adenovirus vector containing the cDNA of wild-type p16 and antisense RNA of uPAR significantly inhibited human mammary epithelial cell capillary formation and vascular endothelial growth factor (VEGF) expression.
|
17273768 |
2007 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
As previously observed for glioblastomas in Europe, there was a positive association between EGFR amplification and p16 deletion (p=0.009), whereas there was an inverse association between TP53 mutations and p16 deletion (p=0.049) in glioblastomas in Japan.
|
16410744 |
2006 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
EGFR amplification and p16 homozygous deletion were significantly more frequent in small cell glioblastomas than in nonsmall cell glioblastomas (EGFR, 46% vs 26%, p = 0.0002; p16 39% vs 25%, p = 0.0167).
|
16957578 |
2006 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The present case is unusual in four aspects: (i) it arose from a low-grade ganglioglioma in the absence of previous radiation or chemotherapy, which is the fourth reported case; (ii) the original tumor showed a high proliferative index on flow cytometry but a low Ki-67 labeling index, implying that the application of flow cytometry might play a certain role in predicting biological and clinical behavior of low grade gangliogliomas; (iii) p53 mutation and deletion appeared in the secondary glioblastoma, which was not shown in the original well-differentiated ganglioglioma; and (iv) the transformed glioblastoma showed p16 inactivation detected by methylation and deletion, which are relatively uncommon genetic events in secondary glioblastomas.
|
14629754 |
2003 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Loss of pRB following p16 expression might severely limit the potential benefit of p16 gene therapy for glioblastoma.
|
12416540 |
2002 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Analysis of homozygous deletion of the p16 gene and correlation with survival in patients with glioblastoma multiforme.
|
12005388 |
2002 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The bicistronic construct (Ad-uPAR/p16)-infected glioblastoma cell lines had significantly lower levels of uPAR and higher levels of p16 than controls.
|
11791179 |
2002 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
All but 4 tumors (84%) showed alterations known to be preferentially involved in the progression of astrocytic tumors to GBM, such as EGFR amplification (44%), P16 deletion (48%), LOH on 10q (64%), PTEN (20%), and TP53 (24%) mutations.
|
11556543 |
2001 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Retroviral mediated p16 and p21 gene deliveries in glioblastomas resulted in more than 90% reductions in tumor growth (92 +/- 26% vs 90 +/- 22%) compared to p53 (62 +/- 18%).
|
11549271 |
2001 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results suggest that the tumor suppressor p16 may exert its antitumor effects through modulation of multiple aspects of glioblastoma phenotypes, including proliferation, invasiveness, and responsiveness to extracellular growth stimuli.
|
11908877 |
2001 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Neither p53 expression nor p21 immunonegativity (52% of AAs and 48% of GBs) correlated with survival. p16 immunostaining was negative in 16% of AAs and in 44% of GBs, and it correlated inversely with survival in both uni- and multivariate analyses. pRb immunostaining was negative only in 8% of both AAs and GBs and the absence of p16 and pRb were mutually exclusive.
|
10896207 |
2000 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
RT-2 rat GBM cell line was used to investigate if the p16 gene induces dominant suppression of glioblastoma growth.
|
10720483 |
2000 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We reconfirmed that p16 hypermethylation may be one of the major mechanisms of tumorigenesis of GBMs and the results between the methylation specific-PCR study and p16 immunostaining had a good correlation.
|
11068994 |
2000 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The human glioblastoma cell line U87MG was doubly transfected with the plasmids pVgRXR and pIND harboring the wild-type p16 gene.
|
10360478 |
1999 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Including 20 additional glioblastoma-derived cell lines we detected that in 19 of the total 31 lines at least one exon was lost bringing the rate of p16 loss in the whole panel to 61%.
|
10536182 |
1999 |
Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We have also shown the presence of heterogeneous cell populations within the glioblastoma masses based on the variety of the mutated p16 sequences.
|
10536183 |
1999 |
Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Five of 25 (20%) glioblastomas had diffuse p16 immunohistochemical positivity.
|
9600204 |
1998 |
Glioblastoma
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Hypermethylation of CpG islands in the 5' region of the p16 gene was identified in only 1 case, suggesting that this alternative mechanism of gene silencing is rarely responsible for loss of p16 expression in glioblastomas.
|
9334810 |
1997 |
Glioblastoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Loss of p16 expression was detected in 11/18 (61%) glioblastomas.
|
9210874 |
1997 |