|
Neoplasms
|
0.100 |
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
|
0.100 |
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
|
0.100 |
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
|
0.100 |
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
|
0.100 |
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
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Immunohistochemical analysis of Her2/neu, p53 and p16 in PDX and PDOX demonstrated maintenance of protein expression found in patient tumors while membranous EGFR overexpression in patient tumor cells was absent in both xenografts.
|
31732509 |
2019 |
|
Neoplasms
|
0.100 |
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
|
0.100 |
Biomarker
|
group |
BEFREE |
Relationship between tumor-associated immune infiltrate and p16 staining over clinicopathological features in acral lentiginous melanoma.
|
30778854 |
2019 |
|
Neoplasms
|
0.100 |
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
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In vivo, miR‑9 depletion decreased the tumor volume and weight and increased p16 expression in the mouse tumor tissues.
|
31081054 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Multivariable analyses showed that age, Charlson comorbidity index, pretreatment and post-treatment sarcopenia, pretreatment hypoalbuminaemia, p16 status and tumour site remained the independent variables predictive of DFS and OS outcomes (all P < 0.05).
|
31185387 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Intrinsic skin ageing is mainly caused by cellular senescence. p16 and p21 are two important tumour suppressor proteins that play essential roles during cell proliferation and ageing through regulating the expression of several genes.
|
31032993 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Median follow-up duration was 5.6 years; 67% of patients had ≥10-pack-year tobacco exposure; 96% of tumors for which p16 data were available were p16 positive.
|
30913911 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We confirmed the loss of the tumor suppressors p16 and NF1 by immunohistochemistry in select cases.
|
30657954 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The expression of cyclin A and p16 and their correlation to histopathological parameters (TNM stage, histological subtype, nuclear grade, tumor size), gender, age, and clinical outcome were studied and analyzed.
|
29135120 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Complete loss of p16 expression and homozygous CDKN2A deletion were observed in 82% and 70% of tumors, respectively.
|
31498175 |
2019 |
|
Neoplasms
|
0.100 |
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
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Expression of tumor suppressor genes p53 and p16 did not significantly change, while p27 was significantly downregulated.
|
30242785 |
2019 |
|
Neoplasms
|
0.100 |
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
|
0.100 |
Biomarker
|
group |
BEFREE |
Multivariate analysis found tumor stage, Karnofsky index, p16, and CD44 as prognostic factors of overall survival and clinical stage, and p16 as a prognostic factor for locoregional control.
|
30552846 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The gene expression level of telomere length-preserving protein RPA1 was significantly higher in the KTx recipients than among the NBL survivors or healthy controls, while the expression of TRF2 and the tumor suppressor gene p16 was significantly higher in the KTX recipients when compared to the controls.
|
31297925 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
As a proof of concept, we considered panels of cancer cells with homozygous codeletions in <i>CDKN2a</i> and <i>MTAP</i>, genes respectively encoding the commonly-deleted tumor suppressor p16 and an enzyme involved in methionine metabolism.
|
31249865 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Immunocytochemical studies on PF cell blocks allow: (a) to distinguish mesothelioma from reactive mesothelial proliferations (e.g. loss of BAP1 nuclear expression, complemented by the demonstration of p16 deletion using fluorescence in situ hybridization, indicate mesothelioma); (b) to separate mesothelioma from adenocarcinoma (e.g. calretinin, CK 5/6, WT-1 and D2-40 are markers of mesothelioma, whereas CEA, EPCAM, TTF-1, napsin A, and claudin 4 are markers of carcinoma); and (c) to reveal tumor origin in pleural metastases of an unknown primary site (e.g.
|
30354850 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Molecular pathological examination of the MDM2, CDK4 and p16 gene in tumors provides the diagnostic gold standard in distinguishing well-differentiated liposarcoma from lipoma.
|
31387607 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The cut-off point for p16 overexpression was diffuse (≥75%) tumor expression with at least moderate (+ 2/3) staining intensity.
|
30873218 |
2019 |