Childhood 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 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Immunohistochemical studies showed substantial overlap in Ki-67 labeling indices, an imperfect correlation between p53 labeling and TP53 mutation status, and complete p16 loss in only two pGBMs but in no PAs.
|
24057326 |
2013 |
Childhood 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 |
Childhood 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 |
Childhood 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 |
Childhood 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 |
Childhood 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 |
Childhood 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 |
Childhood 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 |
Childhood Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Comparisons of tumor suppressor p53, p21, and p16 gene therapy effects on glioblastoma tumorigenicity in situ.
|
11549271 |
2001 |
Childhood 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 |
Childhood 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 |
Childhood 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 |
Childhood 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 |
Childhood Glioblastoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
However, p16 deletions were significantly more frequent in the former (10/28; 36%) than in the latter (1/23, 4%; P = 0.0075), suggesting that this alteration constitutes an additional genetic hallmark of the primary (de novo) glioblastoma.
|
9341929 |
1997 |
Childhood Glioblastoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We found that p16 and a neighboring gene, p15, were often homozygously deleted in glioblastoma multiformes but not in medulloblastomas or ependymomas.
|
7987828 |
1994 |