|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Homozygous deletion of p16 appears to be common in esophageal squamous cell carcinomas but in adenocarcinomas, both gene deletion and transcriptional silencing of p16 were infrequent.
|
9333024 |
1997 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Additionally, we analysed the aberrant methylation frequency of cell cycle inhibitor p16(INK4a) and K-ras gene mutations in the pancreatic samples. p16 inactivation was detected in 43% of adenocarcinomas, in 17% of neuroendocrine tumors, in 18% of pancreatitis and in 63% of pancreas cancer cell lines.
|
12802288 |
2003 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The pancreatic carcinomas with homozygous p16 deletions were largely devoid of nuclear staining (admixed nonneoplastic cells served as internal positive controls); only one adenocarcinoma each reacted with DCS-50 and the polyclonal antibody, and five were positive with ZJ11, suggesting that nonspecific nuclear staining can occur under certain conditions.
|
10937052 |
2000 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
All of these infiltrating adenocarcinomas were previously shown to contain alterations in the p16 gene or its promoter.
|
9788631 |
1998 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The significance of p16 mutations in gastric tumorigenesis was examined by assessing p16 mutations as well as loss of heterozygosity (LOH) on 9p in 13 gastric adenomas and 45 adenocarcinomas.
|
7775254 |
1995 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The p16 coding gene is often mutated in glioblastomas, pancreatic adenocarcinomas and melanoma-prone pedigrees, but, until recently, the significance of these allelic variants has remained unclear.
|
7566978 |
1995 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
All the GNAS-mutated LEGHs were negative for HPV DNA and p16 expression, whereas all the GNAS-mutated adenocarcinomas were positive for HPV DNA and/or p16 expression, implicating GNAS mutations in the development of LEGH and a minor subset of HPV-related cervical adenocarcinomas.
|
24145653 |
2014 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Immunocytochemical studies on PF cell blocks allow: (a) to distinguish mesothelioma from reactive mesothelial proliferations (e.g. loss of BAP1 nuclear expression, complemented by the demonstration of p16 deletion using fluorescence in situ hybridization, indicate mesothelioma); (b) to separate mesothelioma from adenocarcinoma (e.g. calretinin, CK 5/6, WT-1 and D2-40 are markers of mesothelioma, whereas CEA, EPCAM, TTF-1, napsin A, and claudin 4 are markers of carcinoma); and (c) to reveal tumor origin in pleural metastases of an unknown primary site (e.g.
|
30354850 |
2019 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In search of genetic constellations that might indicate the progression of some PILs toward an invasive phenotype, mutations at both the K-ras and p16 genes were sought within PILs of 10 pancreata resected for adenocarcinoma.
|
9187111 |
1997 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Our results show that frequencies of p16 or cyclin D1 polymorphisms in gastric and esophageal ADC do not differ significantly from the healthy control group.
|
16163549 |
2005 |
|
Adenocarcinoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In the rat, 94% of adenocarcinomas induced by the tobacco specific carcinogen 4-methylnitrosamino-1-(3-pyridyl)-1-butanone were hypermethylated at the p16 gene promoter; most important, this methylation change was frequently detected in precursor lesions to the tumors: adenomas, and hyperplastic lesions.
|
9751761 |
1998 |
|
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The significance of p16 mutations in gastric tumorigenesis was examined by assessing p16 mutations as well as loss of heterozygosity (LOH) on 9p in 13 gastric adenomas and 45 adenocarcinomas.
|
7775254 |
1995 |
|
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
As in other tumour types loss of p16 or RB1 appear to be mutually exclusive events in non-functional adenomas and somatotrophinomas respectively.
|
12790793 |
2003 |
|
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Heterozygous allelic loss at 9p was observed in 4 of 25 adenomas (16%); their smallest shared region of deletion was 9p21-pter, which includes both the p16 and p15 genes.
|
8855819 |
1996 |
|
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
DAP-kinase was methylated at a similar frequency in all four stages, whereas hMLH1 and p16 were methylated in cancer samples (20.3% and 42.2%, respectively) more frequently than in intestinal metaplasia (6.3% and 2.1%, respectively) or adenomas (9.8% and 11.5%, respectively).
|
11306456 |
2001 |
|
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Forty-five percent of cancers and 38% of adenomas showed both K-ras mutations and p16 methylation.
|
10220498 |
1999 |
|
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The purpose of this study was to analyze the frequencies of K-ras, p53, and p16 gene mutations, of microsatellite instability (MI) and of loss of heterozygosity (LOH) in GB cancer, dysplasia, and adenoma.
|
11410326 |
2001 |
|
Adenoma
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Whereas LOH of p16 was present in 7 of 14 cases of HGD (50%), it was noted in only 1 of 22 adenomas (5.0%).
|
9490271 |
1998 |
|
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 |
|
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 |
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 |
|
Malignant neoplasm of urinary bladder
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our results suggested that p16 gene mutations, although they occurred at low frequency, are involved in some low-grade and early stage bladder cancers.
|
8747595 |
1995 |
|
Malignant neoplasm of urinary bladder
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Alteration of the p16 and p15 genes, especially coincident homozygous deletion, appears to be a common event in bladder cancer.
|
7563186 |
1995 |
|
Malignant neoplasm of urinary bladder
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
DNA methylation on CpG islands of the p16 (0%, 17% and 21%) and death-associated protein kinase (13%, 33% and 29%) genes, and methylated in tumor-2 (56%, 60% and 76%), 12 (0%, 6% and 30%), 25 (25%, 27% and 35%) and 31 (45%, 56% and 79%) clones was detected in normal urothelium, NBCs and TCCs, respectively.
|
15821584 |
2005 |