|
Astrocytoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Prognostic value of the expression of tumor suppressor genes p53, p21, p16 and prb, and Ki-67 labelling in high grade astrocytomas treated with radiotherapy.
|
10896207 |
2000 |
|
Astrocytoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
CDKN2/p16 inactivation and p16 immunohistochemistry in astrocytic gliomas.
|
9454886 |
1998 |
|
Astrocytoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The cytoplasmic immunoreactivity of p16 appears to be an unfavorable prognostic indicator in high-grade astrocytoma patients.
|
16614947 |
2006 |
|
Astrocytoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We investigated the relationship between homozygous CDKN2/ p16 deletions and cellular proliferation in 50 primary astrocytomas (2 WHO grade I pilocytic astrocytoma, 15 grade II astrocytomas, 20 grade III anaplastic astrocytomas and 13 grade IV GBMs).
|
8857999 |
1996 |
|
Astrocytoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In this study, we examined the expression of Rb and p16 in 170 primary astrocytic gliomas by immunohistochemical techniques, and correlated the expression with overall survival to determine their prognostic value as immunomarkers.
|
11029499 |
2000 |
|
Astrocytoma
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Homozygous deletions of DMBT1 were found in 5% GBMs and 13% low-grade astrocytomas, but not in anaplastic astrocytomas. p16 suffered homozygous deletion in 27% GBMs and 13% low-grade astrocytomas, though no p16 point mutations were found in any of the 50 astrocytomas. p16 promoter hypermethylation was found in 9% GBMs and 6% low-grade astrocytomas.
|
12168116 |
2002 |
|
Astrocytoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results support the hypotheses that functionally wild-type p53 accumulates in some astrocytomas, and that alternative cell cycle checkpoints (such as the p16 pathway) may be more important than p21 in regulating proliferation in astrocytomas.
|
9224526 |
1997 |
|
Astrocytoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Cells with homozygous P16 loss were present in 13 astrocytomas; 14 astrocytomas showed cells with heterozygous loss of P16.
|
10484976 |
1999 |
|
Astrocytoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In this study, we investigated the effects of p16 expression and RA treatment on the expression and distribution of actin, glial fibrillary acidic protein (GFAP), and vimentin within the U343 MG-A astrocytoma cytoskeleton.
|
12237846 |
2002 |
|
Astrocytoma
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
We found p16 methylation in 12 (60%) of the 20 tissues with astrocytoma, but in only 1 of the tissues with oligodendroglioma.
|
19240607 |
2009 |
|
Astrocytoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Immunohistochemical evaluation may be a useful, rapid method to screen astrocytomas for loss of p16 gene expression, regardless of the underlying mechanism leading to p16 gene inactivation.
|
9098651 |
1997 |
|
Barrett Esophagus
|
0.100 |
Biomarker
|
disease |
BEFREE |
The evidence from this systematic review is suggestive of a role for p16 as an epigenetic biomarker for the progression of BO to OADC.
|
29961009 |
2018 |
|
Barrett Esophagus
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Abnormal p16 expression (negative, cytoplasmic, or combined cytoplasmic and nuclear staining) was present in all categories, rising from 68% in BE without dysplasia to 100% in AdenoCa, with cytoplasmic staining only showing a significant correlation with the severity of dysplasia.
|
18665038 |
2008 |
|
Barrett Esophagus
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
The potential role of p16 inactivation by CDKN2A/p16 promoter hypermethylation and/or loss of heterozygosity (LOH) of the CDKN2A gene was investigated in neoplastic progression of Barrett's esophagus.
|
11910361 |
2002 |
|
Barrett Esophagus
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We detected 9p21 loss of heterozygosity, p16 CpG island methylation, and p16 mutations in biopsies from 57%, 61%, and 15%, respectively, of 107 patients with BE.
|
11719461 |
2001 |
|
Barrett Esophagus
|
0.100 |
Biomarker
|
disease |
BEFREE |
Multivariate analyses revealed that only hypermethylation of p16 (odds ratio (OR) 1.74, 95% confidence interval (CI) 1.33-2.20), RUNX3 (OR 1.80, 95% CI 1.08-2.81), and HPP1 (OR 1.77, 95% CI 1.06-2.81) were independently associated with an increased risk of progression, whereas age, BE segment length, and hypermethylation of TIMP3, APC, or CRBP1 were not independent risk factors.
|
15824739 |
2005 |
|
Barrett Esophagus
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We measured p16 (CDKN2A/INK4A) lesions (loss of heterozygosity, mutations, and CpG island methylation), p53 (TP53) lesions (loss of heterozygosity, mutation) and ploidy abnormalities (aneuploidy, tetraploidy) within each Barrett's esophagus segment of a cohort of 267 research participants, who were followed prospectively with cancer as an outcome.
|
15492292 |
2004 |
|
Barrett Esophagus
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We have determined the p16 mutation spectrum for a cohort of 304 patients with Barrett's esophagus, a premalignant condition that predisposes to the development of esophageal adenocarcinoma.
|
19043591 |
2008 |
|
Barrett Esophagus
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The baseline BE and post-RFA NSE were evaluated for immunohistochemical expression of Ki-67 and p53, and genetic abnormalities (DNA-fluorescent in situ hybridization: chromosome 1 and 9, p16 and p53).
|
19491850 |
2009 |
|
Barrett Esophagus
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These data suggest that p16 promoter hypermethylation is a common mechanism of p16 gene inactivation during neoplastic progression in Barrett's esophagus.
|
9834265 |
1998 |
|
Barrett Esophagus
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
It is possible that acid reflux present in BE patients may activate NOX5-S and increase production of reactive oxygen species, which in turn increase p16 promoter methylation, downregulate p16 expression, and increase cell proliferation, thereby contributing to the progression from BE to EA.
|
20576920 |
2010 |
|
Barrett Esophagus
|
0.100 |
Biomarker
|
disease |
BEFREE |
Mutation analysis of the p53, APC, and p16 genes in the Barrett's oesophagus, dysplasia, and adenocarcinoma.
|
9155671 |
1997 |
|
Barrett Esophagus
|
0.100 |
Biomarker
|
disease |
BEFREE |
Chromosomal gains and genomic loss of p53 and p16 genes in Barrett's esophagus detected by fluorescence in situ hybridization of cytology specimens.
|
15017433 |
2004 |
|
Barrett Esophagus
|
0.100 |
Biomarker
|
disease |
BEFREE |
Complete loss of MTAP and p16 was seen in 4 of 25 (16%) patients with Barrett's esophagus, 4 of 18 (22%) with low-grade dysplasia, 5 of 39 (13%) with high-grade dysplasia, 17 of 78 (22%) with invasive adenocarcinoma, and 8 of 36 (22%) of metastases.
|
16224217 |
2005 |
|
Malignant neoplasm of urinary bladder
|
0.100 |
Biomarker
|
disease |
BEFREE |
Genetic evidence in melanoma and bladder cancers that p16 and p53 function in separate pathways of tumor suppression.
|
7747814 |
1995 |