|
Tumor Cell Invasion
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Aberrations of the CDKN2 gene were detected in tumors with lymph node metastasis and muscular invasion (12 of 22; 54%) and in none of stage I tumors (0 of 9.0%; P < 0.05).
|
8752149 |
1996 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Matrigel invasion assays showed that the SNB19 cells expressing exogenous p16 exhibited significantly reduced invasion.
|
9366522 |
1997 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The p16 LI was significantly decreased (P =.0121) in cases with advanced stage. p27 LI was significantly decreased in cases with portal invasion (P =.0409), poor differentiation (P <.0001), larger size (P =.0421), and intrahepatic metastasis (P =.0878, borderline significance).
|
10385644 |
1999 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In univariate survival analysis of the first 5 years, high levels of p16 protein expression (FI > 11.7) (P = 0.005), tumor greatest dimension, World Health Organization (WHO) histologic grade, capsular penetration, seminal vesicle invasion, positive surgical margins, lymph node involvement, and preoperative serum prostate specific antigen > 20 ng/mL all were significant predictors of biochemical failure.
|
10640976 |
2000 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
A higher proportion of p16 positive tumor cells was associated with bigger size, more frequent invasion and higher recurrence of the tumors.
|
11775544 |
2000 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
To investigate the relationship between the expression of p16 gene and the gastric carcinogenesis, depth of invasion and lymph node metastases, and to evaluate the deletion and mutation of exon 2 in p16 gene in gastric carcinoma.
|
11819820 |
2001 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In glioblastoma cell lines deficient for p53, p16(INK4A), and p14(ARF), FAK was inhibited in a dominant-negative manner by the focal adhesion targeting (FAT) domain, reducing invasion.
|
11479198 |
2001 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Gastric cancers showed an inverse correlation between vascular invasion and p16(INK4a) promoter hypermethylation, and adjacent non-tumorous tissues displayed a close association among the grade of chronic inflammation, presence of glandular atrophy and p16(INK4a) promoter hypermethylation. p16(INK4a) expression was markedly decreased in samples with p16(INK4a) promoter hypermethylation when compared with samples without p16(INK4a) promoter hypermethylation.
|
11477571 |
2001 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
The analysis of concomitant P14ARF and TP73 overexpression and clinicopathologic parameters of the tumors showed a statistically significant difference with respect to peritumoral vessel invasion (P = 0.01), lymph node metastasis (P = 0.03), negative ERBB2 expression (P = 0.005), and more advanced pathologic stages (P = 0.03).
|
11319797 |
2001 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Loss of p16 expression is associated with histological features of melanoma invasion.
|
12459643 |
2002 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
We expected that downregulation of uPAR and overexpression of p16 using a bicistronic vector might cause a additive and cooperative effect in the suppression of glioma invasion and growth.
|
11791179 |
2002 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
We examined 73 skin and oral mucosal biopsy specimens immunohistochemically to test this hypothesis. p16 was not detectable in benign hyperplastic lesions, but instead was expressed heterogeneously in some dysplastic and carcinoma in situ lesions and consistently at areas of microinvasion and at superficial margins of advanced SCCs. p16-positive cells in these regions coexpressed the gamma2 chain of laminin 5, identified previously as a marker of invasion in some carcinomas.
|
12875969 |
2003 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Loss of E-cadherin expression followed by expression of the mts1 gene may be an important event for increasing cell proliferation, motility and invasion activity in the progression of GB cancer.
|
12532418 |
2003 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The inhibition of angiogenesis could be related to 1) an increase in genes involved in the inhibition of cell proliferation (p19(INK4), p21(Waf/Cip1),Wnt-5a), the inhibition of cell migration (Rho-GDI 1, alpha E-catenin) and 2) a downregulation of genes involved in angiogenesis (PAI-1, Vitronectin, HoxD3, Notch4) or in cell invasion (Semaphorin E).
|
12624638 |
2003 |
|
Tumor Cell Invasion
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Clinicopathologic correlations showed that CDKN2A methylation was significantly associated with tumors arising in cirrhotic livers; amplifications of 17q was significant in multiple parameters of tumor invasiveness (size, venous invasion, poor cellular differentiation, microsatellite formation); other amplifications (1q, 6p, 10p, and 20p) were also significant in tumor invasion; and deletions (at 1p, 11q, 4q, and 14q) were significant in tumor growth.
|
14499690 |
2003 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Our results show that the p16INK4a gene transfer can inhibit the proliferation and reduce the invasion ability of hepatocellular carcinoma.
|
12508357 |
2003 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Low p14 expression was associated with increased tumour thickness (p=0.008) and increasing level of invasion (p=0.020).
|
15547691 |
2004 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Derailments of this pathway, caused either by lack of pRb1 or p16(INK4A) expression or overexpression of cyclin D1 and/or cdk4/6, are implicated in the deregulation of the cell-cycle machinery, resulting in uncontrolled cell proliferation, tumor heterogeneity, invasion and metastasis.
|
14670612 |
2004 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Concurrent overexpression of p73 and p16INK4a was significantly correlated with metastases in three or more lymph nodes (P = 0.0007), positive immunohistochemistry for p53 (P = 0.014), vascular invasion (P = 0.048) and negative progesterone receptors (P = 0.004).
|
15450420 |
2004 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Furthermore, v-Fos-stimulated invasion is independent of the pRb/p16(INK4a) and p53 tumor suppressor pathways and telomerase.
|
14749371 |
2004 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Up-regulation of p16 at the epithelial-stromal interface in HPV negative keratinizing SCCs is consistent with an HPV-independent response to alterations associated with invasion.
|
15619206 |
2004 |
|
Tumor Cell Invasion
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
To analyze the correlation between the protein expression of p16 and Rb genes in gastric carcinoma (GC), to investigate the role of p16 gene in invasion and lymph node metastasis of GC, and to examine the deletion and mutation in exon 2 of p16 gene in GC.
|
15818729 |
2005 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Before expression of p14ARF can be linked to invasion or invasive phenotype, larger series of (micro-) invasive squamous lesions need to be studied.
|
16406113 |
2006 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
The regression model applied to the group of transplanted patients showed three factors that were independently related to recurrence: vascular invasion (OR 7.5; 95% CI: 1.1-51.8; P=0.039); pRb expression (OR: 11; 95% CI: 1.2-96.9; P=0.03); and p16 expression (OR: 69.7; 95% CI: 5.1-9448; P=0.001).
|
17006321 |
2006 |
|
Tumor Cell Invasion
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Matrigel invasion assays of p16-deleted ESCC cells showed that restoring wild-type p16 activity into the cells significantly inhibits tumor-cell invasion, suggesting that p16 inactivation could be involved in ESCC invasion.
|
17016592 |
2006 |