|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
(Cancer Res 55:2053-2055, 1995), which showed no p16 mutations or homozygous deletions in 18 primary neuroblastomas and nine tumor-derived cell lines.
|
9115582 |
1997 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A survival analysis by p16 status, p53 status, Union for International Cancer Control stage and main treatment modality demonstrated that only p16 status was related to better prognosis in terms of overall survival and disease-specific survival (3-year overall survival, 87 vs. 62%, P = 0.02; 3-year disease-specific survival, 90 vs. 62%, P = 0.02).
|
24470584 |
2014 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A variety of cancer syndromes involving the P16 and BRCA2 genes, for example, also lead to pancreatic cancer, but the gene responsible for familial pancreatic cancer has not been identified so far.
|
9438603 |
1997 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
After further stratification of the cancer group into different clinical-pathologic parameters, there were significant associations in the sex and LN involvement groups in MK gene; alcohol consumption group in p16 gene; age and cell differentiation groups in p21 gene; age and tumour location groups in p53 gene; but we fail to find any significant association with IL-4 gene polymorphisms.
|
16289646 |
2005 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Alterations of p16 and p15 genes have been reported in cancer cell lines and in certain malignant neoplasm.
|
10958872 |
2000 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Although a low percentage of cases of either malignancy have p16 mutations, a higher risk of their development has been reported to occur in certain families with p16 germline mutations.
|
10037301 |
1999 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Although the mechanism of p16 inhibition in cancer remains to be elucidated, senescence and apoptosis may both be important; however, the data suggest that p16-induced growth inhibition can function independently of the retinoblastoma gene product.
|
10854145 |
2000 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
An increasing level of p16 and E6 mRNA transcripts could mean the potential of cervical dysplasia progression to cancer, but further studies should be done to confirm this proposition.
|
24477172 |
2014 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Architectural patterns of p16 immunohistochemical expression associated with cancer immunity and prognosis of head and neck squamous cell carcinoma.
|
28975663 |
2017 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Archival tissue specimens from 223 patients (145 men, 78 women, median age 65 years, range 27-87 years), who presented with cancer in the lungs, were subjected to GP5+/6+ polymerase chain reaction and p16 immunohistochemistry.
|
23571474 |
2013 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Astrocytomas representing all World Health Organization (WHO) grades of malignancy were analyzed in a correlative study using multiplex polymerase chain reaction (PCR) analysis to detect deletions of the p16 gene together with immunohistochemistry to detect loss of the protein in archival specimens of the same tumors.
|
9098651 |
1997 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Autoantibodies to p16 were found in 11.7% in cancer, with significant difference from the normal individuals (p<0.05).
|
17016600 |
2006 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
BAP1 immunohistochemistry and p16 fluorescence in situ hybridization (FISH) have recently been reported as reliable markers of malignancy in biopsies of mesothelioma.
|
26448191 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Based on these studies, we conclude that p16-mediated cytotoxicity is tightly associated with the presence of functional pRb in human cancer cells, and that tumor cells which are mutant or null for p16 are candidates for Adp16 mediated cancer gene therapy.
|
9464545 |
1998 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Bmi1 was clearly overexpressed across a broad spectrum of gastrointestinal cancers, and the expression of Bmi1 increased in a manner that reflected the pathologic malignant features of precancerous colonic tissues (low-grade dysplasia, 12.9 +/- 2.0%; high-grade dysplasia, 82.9 +/- 1.6%; cancer, 87.5 +/- 2.4%). p16 was also strongly expressed in high-grade dysplasia, but not in cancers. p16 promoter methylation was detected only in some Bmi1-positive neoplastic cells.
|
17145814 |
2006 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Both p15 and p16 are located on chromosome 9p21 and alterations have been demonstrated in a variety of human malignancies and human cancer cell lines.
|
9554401 |
1998 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
By contrast, in advanced stages of Kras-driven murine PDAC, loss of p53 or p16 was associated with senescence bypass, and RelA deficiency in this context attenuated cancer cell proliferation and prolonged mouse survival, indicating that RelA enhances tumor progression in established PDAC.
|
27454293 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Cell block analysis is recommended for patients with serosal effusions of unknown origins with the following methods: immunohistochemistry should be performed to validate the mesothelial origin, and p16 FISH should be performed to confirm malignancy.Diagn.Cytopathol.2016;44:591-598.
|
27079839 |
2016 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Combined evaluation by single clone and whole chromosome analysis plus 'moving average (MA) approach' enabled us to confirm most of the genetic abnormalities previously identified to be associated with glioma progression, including +1q32, +7, -10, -22q, PTEN and p16 loss, and to disclose new small genomic regions, some correlating with grade malignancy.
|
16247447 |
2006 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Consequently, restoration of wild-type p53 or p16 functions is seen as a particularly promising approach for cancer gene therapy.
|
16984510 |
2006 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Conversely, p53 mutation is more often associated with nonendometrioid cancer; others being inactivation of p16 and/or overexpression of HER-2/neu.
|
19078924 |
2009 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Correlation between DNA alterations and p53 and p16 protein expression in cancer cell lines.
|
15901131 |
2005 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Cyclin D1 protein dysregulation at last follow-up alone and in combination with p16 loss was associated with histological progression and cancer development (P < 0.01).
|
11595705 |
2001 |
|
Malignant Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Deletions, mutations and functional inactivation of p16 occur with a frequency second only to p53 in most human malignancies.
|
12145426 |
2002 |
|
Malignant Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Detection of promoter hypermethylation of cancer-related genes may be useful for cancer diagnosis or the detection of recurrence. p16, an inhibitor of the cyclin D-dependent protein kinases, is a classical tumor suppressor gene, and its inactivation is closely associated with carcinogenesis. p16 hypermethylation could be detected in each stage, which is consistent with the finding that aberrant methylation of p16 is a very early event in carcinogenesis.
|
12907744 |
2003 |