|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Furthermore, Tbx3 expression was found to be suppressed by AFLL when the expression of tumor suppressor genes p14 and p53 were activated.
|
20702496 |
2011 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
This pathway was recapitulated by deregulated Wnt/T-cell factor signaling, with elevation of the tumor suppressor p14ARF, and reduced expression of the p53 antagonist, MDM2.
|
15958644 |
2005 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
80% (28/35) of patient tumors had high p16 expression using conventional IHC.
|
25271758 |
2014 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
In fact K-ras point mutations were frequently recognised in tumors at early stage while p16(INK4A) inactivation prevailed in tumors at advanced stage ( P=0.0063).
|
15013580 |
2004 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Along these lines, activation of tumor suppressor mechanisms that inhibit the cell cycle (e.g. p16(INK4a) and p53) in response to DNA damage and other age-promoting stimuli has taken center stage in immune-aging research.
|
19535234 |
2009 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
The methylation of the p16 gene promoter could significantly reduce p16 expression, losing its tumor suppressor activity and promoting the development of cervical cancer.
|
28617556 |
2017 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Genomic instability, mutations and expression analysis of the tumour suppressor genes p14(ARF), p15(INK4b), p16(INK4a) and p53 in actinic keratosis.
|
18331779 |
2008 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
DAPK1 level in the tumour was significantly higher in females than in males, the MGMT and p16 levels were lower in the tumours with lymph node metastasis (N1 + N2) than in N0 samples.
|
28421310 |
2017 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Unexpectedly, metastasis was not observed in mice that developed spindle carcinomas, which expressed high levels of the tumour suppressors p16(Ink4a) and p19(Arf) , encoded by Cdkn2a, a gene frequently deleted in human SCCs.
|
27447534 |
2016 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
To investigate if Mts1/S100A4 has a significant role on brain tumor progression, we made quantitative RT-PCR analysis for the expression of S100A4/Mts1 in various grades of astrocytic tumors.
|
17223348 |
2007 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
These results: (i) demonstrate that the phosphorylase deficiency is distributed among almost all the most important human cancers; (ii) confirm and extend the tumor types were p16INK4 gene inactivation is observable and (iii) suggest that deletions at 9p21 (in humans) or at syntenic chromosomes (in other species) might represent a general mechanism of p16INK4 gene loss of function and possibly, in turn, of cancer development and/or progression.
|
7898924 |
1995 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Additional features were detected in this tumor that are known to be associated with an unfavorable prognosis, including loss of p16 expression and gains of chromosomes 1q and 12.
|
22007764 |
2012 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Univariate analysis was followed by multivariate analysis according to a Cox model. p14(ARF), p16(INK4A) and PTEN expressions, and 10p 10q23, 10q26 and 13q LOH for the entire cohort, hTERT expression for high-grade tumours, EGFR for glioblastomas, 10q26 LOH for grade III tumours and anaplastic oligodendrogliomas were found to be correlated with overall survival on univariate analysis and age and grade on multivariate analysis only.
|
18506188 |
2008 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
At least four distinct groups of tumors were identified sharing a common histology but displaying different molecular/cytogenetic patterns: (a) 19% were HPV-positive SCCs whose lack of alterations of the investigated genes could explain their particular natural history, which requires less aggressive treatment; (b) 37% were HPV-negative SCCs carrying TP53 mutations, which may be more effectively treated by drugs acting through p53-independent apoptosis; (c) 34% were HPV-negative SCCs carrying wild-type TP53 and loss of 9p21 (p16INK4a and p15INK4b) and/or cyclin D1 overexpression that justify treatment with DNA-damaging drugs followed by cell cycle inhibitors; and (d) 10% were HPV-negative lacking tumor suppressor genes and cell cycle alterations.
|
17121883 |
2006 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
We highlight the difficulty in distinguishing tumour cell necrosis from infarct-type necrosis and the limited utility of p16 immunohistochemical expression in the diagnosis of leiomyosarcoma.
|
23240674 |
2013 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
No detectable alterations were observed in the majority of cases with overexpressed p14ARF mRNA, but 77% of tumors with decreased expression presented at least one of these genetic/epigenetic alterations.
|
11494155 |
2001 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Moreover, loss of p16 expression in pancreatic malignancy was significantly associated with histological grade (G1 versus G2 and G3, P < 0.01) but not with sex, age, clinical stage, tumor location, or resectability.
|
9815833 |
1997 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
These results demonstrate that p16 expression patterns differ based on tumor histology and origin.
|
9333024 |
1997 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
We concluded that the paradoxical expression of CDKN2A in neuroblastoma cannot be explained by inactivation of the tumor-suppressor gene CDKN1B or overexpression of the oncogene ID2.
|
15390183 |
2004 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
p16INK4a expression and absence of activated B-RAF are independent predictors of chemosensitivity in melanoma tumors.
|
18953432 |
2008 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Multivariate Cox regression analysis could identify patients with low FGFR3 and high CDKN2A/p16 expression (log rank (LR) χ<sup>2</sup> = 10.69; P = .0048) as well as tumor size ≥3 cm (LR χ<sup>2</sup> = 6.03; P = .0141) as independent predictors for PFS.
|
29525349 |
2018 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Mechanistically, these effects were mediated by attenuation of cell cycle progression, as Western blot analyses demonstrated upregulation of the tumor suppressor p21/CDKN2A and downregulation of the cell cycle regulator Cyclin D1 as well as reduced levels of phosphorylated ribosomal protein s6 (pRPS6) and retinoblastoma protein (pRb).
|
31018208 |
2020 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Nuclear and cytoplasmic staining intensity of samples within tumor cells and normal skin tissue illustrates different mRNA and protein expression of p16 gene. mRNA of p16 gene and the expressed protein induce cell cycle proliferation and involve both tumor tissue as well as normal skin tissue.
|
18760195 |
2008 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
The alteration of P16 and RBSP3 was synergistic and showed association with overexpression of p-RB1 in tumors and associated with poor prognosis of patients.
|
27458253 |
2016 |
|
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Ectopic expression of SCCRO in glial progenitor cells resulted in lower-grade gliomas in Ink4a(-/-) mice, whereas its expression in Ink4a(-/-)/PTEN(-/-) background produced high-grade glioblastoma-like lesions that were indistinguishable from human tumors.
|
20563250 |
2010 |