The expression of p16 and cyclin D1 protein had correlation with the tumor size, lymph node metastasis and tumor-node-metastasis stage of cardiac carcinoma (P<0.01).
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.
In head and neck cancer patients with low tumourp16 expression, SMO expression was an independent factor for overall survival (HR = 0.49; 95% CI = 0.24-0.98; P = 0.043) and disease-free survival (HR = 0.45; 95% CI = 0.22-0.96; P = 0.037).
FHIT was related to HCC tumor-node-metastasis (TNM) staging, the differentiation degree in Edmondson-Steiner grading, lymph node metastasis and portal vein thrombosis (P<0.05 in all comparisons), whereas, p16 was associated with tumor size and the differentiation degree in Edmondson-Steiner grading (P<0.05 in all comparisons).
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.
We retrospectively examined survival of 107 patients with locally advanced OPSCC after radiotherapy alone (n = 43) or chemoradiotherapy (n = 64) with respect to tumorp16 and HPV DNA status, using Cox's proportional hazard model.
Association of expression levels of tumor suppressor proteins p53 and p16 and inflammatory factors in simulated weightlessness with the degree of lumbar disc degeneration of rats was investigated.
We also found that deficiency of Np95 in NS/PCs increased the expression of tumor suppressor genes p16 and p53, and confirmed that expression of these genes in NS/PCs recapitulates the phenotype of Np95-deficient NS/PCs.
Reprogrammed metabolism and cell cycle dysregulation are two cancer hallmarks. p16 is a cell cycle inhibitor and tumor suppressor that is upregulated during oncogene-induced senescence (OIS).
The aim of the study was to evaluate the expressions of Serpin A1 in LS, premalignant vulvar lesions, and vSCC using immunohistochemistry (IHC) and serum analysis, and to compare Serpin A1 stainings to the tumor markers p53 and p16.
By immunohistochemistry, the tumor was p53-wild type (DO-7 clone), diffusely positive for p16 (block positivity), and showed retained expression of PTEN, MSH2, MSH6, MLH1, and PMS2.
IHC indicated that the positive expression rate of p16 in the tumor tissues was significantly lower than that in the tumor-adjacent tissues [34.67% (26/75) vs. 85.33% (64/75), p<0.05].
Furthermore, p16 protein overexpression was significantly associated with the Dukes stage, lymph node metastasis, tumor location, and Tumor Lymph Node Metastasis-stage of colorectal cancer.
The human papillomavirus (HPV) status of the tumor samples was assessed with in situ hybridization, the MassARRAY HPV multiplex polymerase chain reaction assay, and p16 immunostaining.
Tumor suppressor gene p16 promoter hypermethylation has been widely studied in colorectal cancer (CRC), yet its clinicopathological significance remains controversial.
Patients with p16 positive tumors or tumors with a low intensity of fibronectin showed significantly higher overall survival in univariable regression.
We identified 326 DNA HPV-positive VSCC with at least 1 cm of skin adjacent to the invasive tumor and analyzed HPV typing, HPV E6*I mRNA, and p16 immunohistochemistry in all cases.
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.