Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
When compared to a reference of tumor tissue p16 IHC in 783 OPSCC patients, the clinic-HPV<sub>sero</sub> model incorporating a composite of 20 HPV serological antibodies (HPV<sub>sero</sub> ) and 4 clinical factors (c-index: 0.96) performed better than using HPV<sub>sero</sub> (c-index: 0.92) or HPV<sub>mi</sub> (c-index: 0.76) alone.
|
31269236 |
2020 |
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 |
Biomarker
|
group |
BEFREE |
Tumor histology correlated well with p16 positivity (P<.001) and p16 IHC accurately predicted the presence of HPV in 25/26 (96%) cases.
|
31698006 |
2020 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
DNA mismatch repair protein expression studies disclosed loss of nuclear immunostaining of MSH6 protein, pointing to the possibility of an underlying rare MSH6 variant of the Muir-Torre syndrome, not yet described in the ophthalmic literature. p16 nuclear positivity was also found in the tumor cells, indicating the possible role of high-risk human papillomavirus as an additional factor in the genesis of the tumor.
|
31557488 |
2020 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
HPV 16 and/or 18 were detected in 156 (80%) tumors. p16 was positive in 186 (96%) carcinomas, but eight tumors (4%) were negative for p16 (seven squamous cell carcinomas, one adenocarcinoma); 5/8 caused by HPV 16 and/or 18.
|
31492932 |
2020 |
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Seven tissue microarrays were constructed. p16 protein expression was studied in 114 cases, of which 35/114 (30.7%) cases showed strong expression and the majority of them had ER-positive tumor (57.6%), and it was statistically significant (P < 0.0074).
|
31603125 |
2020 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
Palbociclib is a CDK4 inhibitor with preclinical antitumor efficacy in tumors with P16/CDKN2A loss.
|
30979737 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
Furthermore, methylated RASSF1A and p14/ARF were associated with the grade of CRC but not associated with the age of patients, family history, or tumor location.
|
30989570 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
Additional FISH analyses detected a 9p21/CDKN2A double deletion, frequently reported in melanomas but not in nevi, in the tumor initially diagnosed as a Spitz nevus with a favor malignant p16-Ki-67-HMB45 score.
|
28362709 |
2019 |
Neoplasms
|
0.500 |
GeneticVariation
|
group |
BEFREE |
TERT promoter mutation, H3F3A mutation, CDKN2A loss) in this tumor group.
|
30298540 |
2019 |
Neoplasms
|
0.500 |
GeneticVariation
|
group |
BEFREE |
The total mutational burden was similar between human papillomavirus (HPV)-negative vs. positive tumors, although TP53, CDKN2A and CCND1 gene alterations occurred more frequently in HPV-negative tumors.
|
29747488 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
OncoScan analysis showed genetic changes that define field cancerization of the p16 negative tumor as revealed by mosaicism in both loss of heterozygosity and copy number alterations in cancer-associated genes located on 3p, 7p, 9p 11q, and 17p.
|
30552721 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
<i>K</i><sub>ep</sub> kurtosis was significantly higher in p16 tumors, and <i>V</i><sub>e</sub> min was significantly lower in p16 tumors compared to the p16 negative tumors.
|
30718984 |
2019 |
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
The tumor expressed S100 and was negative for CD31, CD34, desmin, and smooth muscle actin.The expression of p16 was preserved.
|
30421509 |
2019 |
Neoplasms
|
0.500 |
GeneticVariation
|
group |
BEFREE |
Our study pointed out the utmost relevance of CDKN2A homozygous deletion as an adverse prognostic factor in the 2 broad categories of IDH-mutant gliomas stratified on 1p/19q codeletion and suggests that the grading of these tumors should be refined.
|
31832685 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
An Oncolytic Adenovirus Vector Expressing p14 FAST Protein Induces Widespread Syncytium Formation and Reduces Tumor Growth Rate <i>In Vivo</i>.
|
31193718 |
2019 |
Neoplasms
|
0.500 |
GeneticVariation
|
group |
BEFREE |
This study showed mutations in the tumor suppressor CDKN2A gene and the NRAS oncogene in 62.5% and 75%, respectively of the samples that had mutations in the ABCB5 gene.
|
30905807 |
2019 |
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
A total of 28 studies with 2612 nasopharynx cancer patients were included in the meta-analysis. p16 protein expression was significantly associated with the risk, lymph node metastasis, TNM-stage (tumor-node-metastasis), distant metastasis, and T stage of nasopharynx cancer (Risk, OR = 17.82, 95% CI = 11.20-28.35; Lymph node metastasis, OR = 2.11, 95% CI = 1.42-3.14; TNM-stage, OR = 2.25, 95% CI = 1.54-3.28; Distant metastasis, OR = 3.43, 95% CI = 1.55-7.58; T-stage, OR = 1.72, 95% CI = 1.27-2.33).
|
30882625 |
2019 |
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
The tumor suppressor gene FHIT is lowly expressed in breast cancer tissues and positively associated with the expression of the multi-tumor suppressor gene p16.
|
30941950 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
Distinct Roles of Direct Transduction Versus Exposure to the Tumor Secretome on Murine Endothelial Cells After Melanoma Gene Therapy with Interferon-β and p19Arf.
|
30848981 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
Intraperitoneal injection of bexarotene significantly decreased expressions of CCL22, CXCL5, CXCL10, and p19 in the tumor microenvironment.
|
31616630 |
2019 |
Neoplasms
|
0.500 |
AlteredExpression
|
group |
BEFREE |
Comparison of P16 expression in OSCC tumors with different degrees of promoter methylation further suggest the relationship of methylation rate and down-regulation of P16 expression.
|
30511108 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
Cancers rewire metabolism to facilitate proliferation; however, it is not well appreciated how this enables senescence bypass.Recent work by Buj et al. demonstrates that loss of the tumor suppressor p16 engages a mTORC1-dependent increase in nucleotide pools to override senescence.
|
31699584 |
2019 |
Neoplasms
|
0.500 |
Biomarker
|
group |
BEFREE |
The p16Ink4a plays an important role in tumor suppression, whereby its deletion, mutation, or epigenetic silencing is a frequently observed genetic alteration in prostate cancer.
|
30677079 |
2019 |
Neoplasms
|
0.500 |
GeneticVariation
|
group |
BEFREE |
The median tumor mutation burden for GBC patients was 5.4 (range: 0.8-36.74) mutations/Mb, and the most common mutations were in TP53 (73%), CDKN2A (25%) and PIK3CA (20%).
|
31700903 |
2019 |