|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
These results show a critical role of CDKN2B inactivation in pancreatic carcinogenesis, and provide a useful adult animal model by genetic engineering via lentiviral delivery.
|
28892048 |
2018 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In a model of ectopic expression of miR-18b and CDKN2B, CDKN2B overexpression antagonized the effects of miR-18b <i>in vitro</i> and <i>in vivo</i> The data show that miR-18b is involved in CRC carcinogenesis through targeting CDKN2B.
|
28784723 |
2017 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The degree to which the associated CDKN2B-encoded p15 loss contributes to human tumorigenesis is unclear.
|
26183406 |
2015 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
This study investigated the potential roles of CDKN2B-related piRNA in leukemia cells to provide a potential tumorigenesis model of leukemia.
|
26205624 |
2015 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
HBV infection is associated with p14 (ARF) , p15 (INK4B) , p16 (INK4A) , and RB gene methylation (P = 0.048, 0.035, 0.02); HBV-DNA replication is associated with p14 (ARF) , p15 (INK4B) , p16 (INK4A) , and RB gene methylation (P = 0.048, 0.035, 0.02); high rate of p14 (ARF) , p15 (INK4B) , and p16 (INK4A) in HCC with HBV infection suggests that HBV-induced hypermethylation may be one of the mechanisms of HBV involved in hepatocellular carcinogenesis.
|
24254306 |
2014 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In the present study, the methylation patterns of three genes [p16 (INK4A), p15 (INK4B), and adenomatous polyposis coli (APC)] were assessed in patients with gastric adenocarcinoma from Pará state in order to identify possible molecular markers of gastric carcinogenesis.
|
23504555 |
2013 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
This mechanism would provide an increased advantage for bypassing senescence, sustaining the requirements for the proliferation of stem and/or progenitor cell populations or inappropriately leading to oncogenesis through the aberrant saturation of the INK4b-ARF-INK4a locus by PcG complexes.
|
21828241 |
2011 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Indeed, we find that reexpression of p15 in tumor-derived cells significantly attenuates the tumorigenic potential of these cells, indicating that p15 loss may be a critical event in tumorigenesis triggered by complex DSBs.
|
20663777 |
2010 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
The Ink4a-Arf-Ink4b locus has a crucial role in both cellular senescence and tumorigenesis.
|
18836456 |
2008 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
These findings suggest that variable expression levels of cell-cycle inhibitor genes CDKN2A, CDKN2B, and CDKN1B due to regulatory polymorphisms could indeed influence the risk of childhood pre-B ALL and contribute to carcinogenesis.
|
17008550 |
2007 |
|
Carcinogenesis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Our results suggest that methylation of the p15(INK4b) gene contributes to the process of carcinogenesis in colorectal cancer as well as p16(INK4a) and is useful as a prognostic factor in the early stage.
|
16872319 |
2006 |
|
Carcinogenesis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Our results suggest that epigenetic alterations in p15INK4b but not p16INK4a have an important role in ovarian carcinogenesis and that mechanisms other than methylation may exist to reduce gene expression of p15INK4b in ovarian cancer.
|
16000597 |
2005 |
|
Carcinogenesis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Our results suggest that inactivation of the RB1 pathway may play a causal role in pituitary tumorigenesis, with hypermethylation of the p16(INK4a) gene being the most common deregulation, and further provide evidence that RB1 and p16(INK4a) methylations tend to be mutually exclusive but occasionally coincide with p15(INK4b) methylation.
|
15892297 |
2005 |
|
Carcinogenesis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Association of low p16INK4a and p15INK4b mRNAs expression with their CpG islands methylation with human hepatocellular carcinogenesis.
|
15112341 |
2004 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The results suggest that p15 gene methylation can be induced by chronic smoking and drinking and may play a role in the very early stages of carcinogenesis in HNSCC.
|
15221997 |
2004 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Moreover, p16 and p15 gene deletion was related to tumor progression and might have a role in bilharzial bladder carcinogenesis.
|
15590562 |
2004 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Expression of the TGF-beta downstream target gene p21(waf1), regulation of the p15(ink4b) promoter, anchorage-independent growth, and tumorigenesis were examined.
|
12429655 |
2002 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Although the number of cases we analyzed was not large, alterations identified in the Rb, p53, p16, p15 and p14 genes are of significance and might be associated with tumorigenesis in NK cell neoplasms.
|
11676855 |
2001 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In order to explore the possibility of a selective deregulation of p15(INK4b) in human lung carcinogenesis, we studied p15(INK4b) status in neuroendocrine (NE) lung tumours where homozygous deletions of the p16(INK4a)/p14(ARF) locus are rarely observed.
|
11641784 |
2001 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The INK4A and INK4B loci are located at 9p21 and have been implicated in the tumorigenesis of various human malignancies.
|
11369056 |
2001 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The P15 gene appeared to play a lesser role in tumorigenesis of these tumors.
|
10432931 |
1999 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Our data suggest that inactivation of p15 and p16 genes could be one of the major pathways responsible for oxystress-induced carcinogenesis.
|
10391689 |
1999 |
|
Carcinogenesis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Our results in studies with cell lines and primary MM support the fact that hypermethylation of p16 and p15 plays an important role in MM tumorigenesis.
|
10492069 |
1999 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Malignant mesothelioma expresses pRb, which, together with the cytogenetic data, suggests the involvement of CDKN2A and/or CDKN2B in its tumorigenesis.
|
9466670 |
1998 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
We conclude that mutations of the p16INK4A and p15INK4B genes are not required for tumorigenesis of the pituitary gland.
|
9037130 |
1997 |