Although overall survival (OS), recurrence free survival (RFS) and metastasis free survival (MFS) had no significant differences between the p16 positive and negative patients, p16 negative patients (cut off value 25%) had more RFS in the buccal mucosa cancer (p= 0.03) than the p16-positive patients.
These results suggest that p16, has novel anticancer properties capable of suppressing cancer cell migration and invasion and pharmacologic restoration of p16 level in stromal fibroblasts may be exploited as therapeutic strategy to prevent nodal or distant metastasis.
Age, smoking, N3 disease, T4 disease, and a negative p16 status were associated with the development of distant metastases in patients with squamous cell cancers of the oropharynx treated definitively with concurrent chemoradiation.
Methylation frequency of CLDN11 (OR, 25.56; 95% CI, 2.32-281.66; p = 0.008), MGMT (OR, 4.64; 95% CI, 1.98-10.90; p = 0.0004), p16 (OR, 4.31; 95% CI, 1.33-13.96; p = 0.01), and RASSF1A (OR, 10.10; 95% CI, 2.87-35.54; p = 0.0003) was significantly higher in metastasis melanoma compared with controls.
Immunohistochemical expression of p16 in ovarian tumors can guide the diagnosis of metastasis from HPV-related cervical cancer, but p16 positivity is nonspecific.
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).
Immunohistochemical examination revealed diffuse CK19 and p16 expression, and patchy CK7 expression in the solid components of primary and metastatic tumors.
HPV tumor status testing may be performed by surrogate marker p16 immunohistochemistry either on the primary tumor or from cervical nodal metastases only if an oropharyngeal primary tumor is present.
Differentiation degree, clinical stage, metastases of nearby lymph nodes and distant metastasss were negatively related with p16 gene expression (p less than 0.05).
This resistant population rapidly expanded after the initiation of MEKi + CDK4i therapy and persisted in all successive samples even after immune checkpoint therapy and distant metastasis.
A tendency toward mutual exclusivity was seen between multiple genes in intrahepatic cholangiocarcinoma including <i>TP53:IDH1, IDH1:KRAS, TP53:BAP1</i>, and <i>IDH1:FGFR2</i> Alterations in CDKN2A/B and ERBB2 were associated with reduced survival and time to progression on chemotherapy in patients with locally advanced or metastatic disease.
In univariate analysis for CSS, we found that four of the tested markers, namely high expression of p53 (P = .001), EGFR (P = .003), cyclin A2 (P = .005) and low expression of p16 (P = .019), along with clinical stage (P < .001), tumour size (P < .001), presence of nodal metastasis (P < .001) and perineural permeation (P = .039) were related to decreased survival.
MMP9, OPN, TP53 and CDKN2A were the identified markers that were expressed in a similar pattern in early embryonic development and cancer development & invasion suggesting that these genes are activated during embryogenesis and might be re-expressed in cancer metastasis.
In a separate analysis of 347 primary PanNETs, we found loss or deletion of DAXX and ATRX, disruption of SETD2 function (based on loss of H3 lysine 36 trimethylation), loss of ARID1A expression or deletions in CDKN2A in 81% of primary PanNETs with distant metastases.
A primary HNcSCC should be considered in p16 positive neck node metastases in regions with high prevalence of HNcSCC. p16 expression is not associated with improved survival in HNcSCC.
The expression of both CtBP2 and p16INK4A were significantly related to histological differentiation (P < 0.01 and P = 0.004, respectively) and metastasis (P = 0.046 and 0.047, respectively).
RGS4 and P16 protein expressions were not associated with tumor, node metastasis (TNM) and pathological typing of nephroblastoma, but they were lowly expressed in patients with high metastasis (p < 0.05).
Patients with oropharyngeal carcinoma positive for human papillomavirus or p16 lived longer after locoregional failure compared with patents with oropharyngeal carcinoma negative for human papillomavirus or p16 (median survival, 36.5 vs 13.6 months; P = .007) but not after distant metastasis.
TWIST was the key player in promotion of pancreatic cancer development and metastasis under a hypoxic condition through interaction with Ring1B and EZH2 to regulate expression of E-cadherin and p16 proteins in pancreatic cancer cells.