Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Remarkably, deletion of the Cdkn2a gene in p53(R172H) -induced SCCs promoted a dramatic increase in metastasis rates and a shorter survival in mice that developed these tumours, compared with those observed in mice with tumours in which Cdkn2a was deleted in the presence of a p53 loss-of-function mutation or wild-type p53.
|
27447534 |
2016 |
Neoplasm Metastasis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
There was no statistically significant difference between p16 expression in CRC and nodal metastasis.
|
27976639 |
2016 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
The LOH in the coding region of CDKN2A, at D9S974 and D9S942, was associated with a higher pT-stage (p = 0.004) and metastasis (p = 0.006, both markers).
|
27682877 |
2016 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Several genetic and epigenetic aberrations of CDKN2A lead to enhanced tumorigenesis and metastasis with recurrence of cancer and poor prognosis.
|
27428416 |
2016 |
Neoplasm Metastasis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In contrast, in basal-like tumours, c-MYC showed positive association with Cyclin E (P=0.003) and p16 (P=0.042) expression only. c-MYC was an independent predictor of a shorter distant metastases-free survival in luminal A LN+ tumours treated with endocrine therapy (ET; P=0.013).
|
26954716 |
2016 |
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In the multivariate analysis, non-metastatic disease (P=0.033) and p16 positivity (P=0.005) have shown their prediction value for OS while non-metastatic disease (P=0.002), HPV positivity (P=0.041) and negative resection margin predicted a better recurrence-free survival.
|
27279281 |
2016 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
STAT3 and CDKN2A deletions co-occurred with high frequency in PCa metastases.
|
26198641 |
2015 |
Neoplasm Metastasis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Suppression of endogenous miR-429 promoted cell growth and metastasis. miR-429 was shown to directly target the 3' untranslated regions of B-cell-specific Moloney murine leukemia virus insertion site 1 (BMI1) and E2F transcription factor 3 (E2F3) transcripts, regulating their expression, as well as that of the downstream epithelial-to-mesenchymal transition markers E-cadherin, N-cadherin, vimentin, p14, and p16.
|
25953723 |
2015 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Previous studies implicating aberrant AKT signaling in human melanoma metastases led us to evaluate the effect of activated AKT1 expression in non-metastatic BRAF(V600E)/Cdkn2a(Null) mouse melanomas in vivo.
|
26565903 |
2015 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
In a multivariable analysis (Cox regression model), the parameters that were statistically associated with a poorer overall survival were the presence of metastases at diagnosis (P = 0.014), gastrointestinal histology (P < 0.0001), PTEN (P < 0.0001), and CDKN2A alterations (P = 0.0001).
|
25928476 |
2015 |
Neoplasm Metastasis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
It has been reported that genetic inactivation of P16 drives cancer growth and metastasis, however, whether P16 DNA methylation is truly a driver in cancer metastasis remains unknown.
|
26592237 |
2015 |
Neoplasm Metastasis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
The frequency of p16 methylation was significantly higher in GC tissues (85.9%; 79/92) than that in paired PCHNTs (12.0%; 11/92) (P<0.0001). p16 methylation correlated closely with lymph node metastasis, peritoneal metastasis, TNM stage, et al (all P<0.05).
|
24817951 |
2014 |
Neoplasm Metastasis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
p14ARF repression induced by promoter methylation associated with metastasis in esophageal squamous cell carcinoma.
|
22973996 |
2014 |
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The presence of metastatic disease at diagnosis (p = 0.03), distant recurrence disease (p = 0.006) and shorter distance recurrence-free survival (p = 0.05) was associated with lack of p16.
|
24606815 |
2014 |
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
These findings provide insight into the mechanism of DDR engagement by activated oncogenes and highlight genetic interactions between the DDR and Ink4a-Arf pathways in suppression of oncogene-driven tumorigenesis and metastasis.
|
24120666 |
2013 |
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Loss of p16 immunolabeling was associated with lymphatic invasion (P = 0.012) and postoperative widespread metastases (P < 0.001).
|
23470568 |
2013 |
Neoplasm Metastasis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
We immunohistochemically analyzed p16 expression in surgically resected aggressive cutaneous head and neck SCC primaries and their nodal metastases from 24 patients to determine the potential overlap of p16 expression outside of the oropharynx.
|
23108906 |
2013 |
Neoplasm Metastasis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
The methylation of p16 gene was positively associated with metastasis, a high AMES (age, metastasis to distant sites, extrathyroidal invasion, size) risk group (p < 0.05) and advanced pathological tumor-lymph node-metastasis stages.
|
23497965 |
2013 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Three miRNA sets were significantly associated with overall survival (miR-107, miR-151, miR-492; P = 0.0002), disease-free survival (miR-20b, miR-107, miR-151, miR-182, miR-361; P = 0.0001), and distant metastasis (miR-151, miR-152, miR-324-5p, miR-361, miR492; P = 0.0087), which retained significance even after adjusting for p16 status.
|
23459718 |
2013 |
Neoplasm Metastasis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Positive p14ARF expression was significantly associated with the following variables: shorter cancer-specific survival (P=0.04) and shorter disease-free survival (P=0.02), presence of perineural invasion (P=0.037), vascular invasion (P=0.047), and node metastasis (P=0.031).
|
22878614 |
2013 |
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The contribution of aberrant methylation alterations of BMP6, BRCA1 and P16 genes in lymph node metastasis might provide a further clue to establish useful biomarkers for screening metastasis.
|
22695536 |
2012 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Instead, we identified deletion of the p16 (CDKN2A) and retinoblastoma (RB1) genes as likely causal events leading to increased AURKA and CINSARC gene expression, to chromosome rearrangement, and ultimately to metastasis.
|
22167411 |
2012 |
Neoplasm Metastasis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The upregulated genes were related to (i) hypoxia-inducible factor (HIF) molecules (CA9, HIF2A, and GLUT1), (ii) angiogenesis (CDH5, VEGFR1, EDNRA, ANGPT2, CD34, VEGFR2, VEGFA, and ANGPT1), (iii) the processes of epithelial-mesenchymal transition (VIM) and/or metastasis (LAMA4 and CXCR4), (iv) growth factors and receptors (PDGFB, IRS1, and ERBB1), or (v) cell cycle (CCND1 and CDKN2A).
|
22461457 |
2012 |
Neoplasm Metastasis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Intratumor heterogeneity for expression of P16INK4a and MGMT may reflect intratumor heterogeneity for methylation patterns and thereby in general explain the moderate sensitivity of our marker panel for detection of metastases.
|
22266550 |
2012 |
Neoplasm Metastasis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
The alterations of p16 gene may play a major role in malignancy and development and metastases of buccal carcinoma and may be an excellent marker of aggressive clinical behavior.
|
22429295 |
2012 |