A previous analysis of these NSCLC samples for p16 gene alterations revealed that the three cases with homozygous deletions of the p15 gene also have homozygous deletions of the p16 gene.
Additionally, in the analysis of the studies following REMARK guidelines more rigorously, p16 hypermethylation had unfavorable impact on OS of NSCLC (HR 1.79, 95% CI: 1.35-2.39) and CRC (HR 1.96, 1.16-3.34), and on DFS of NSCLC (HR 2.12, 95% CI: 1.21-3.72) and head and neck cancer (HR 2.24, 95% CI: 1.35-3.73).
Analysis of the region that encodes for p16 by deletion mapping, a polymerase chain reaction (PCR)-based methylation assay and PCR single-strand conformation polymorphism (SSCP) analysis revealed that deletions and transcriptional silencing by methylation might represent the main mechanisms of CDKN2/p16ink4a inactivation in NSCLCs.
Despite the fact that p16 is important in NSCLC carcinogenesis, the data obtained in our study do not allow the prognostic impact of this biological marker to be established.
Expression levels of cyclin D1, cyclin A2, cyclin E, and p16 proteins that are involved in the G1-to-S phase progression of cell cycle were analyzed using immunohistochemistry in formalin-fixed paraffin-embedded tissues from 372 samples of stage II-IIIA NSCLC.
If p16 inactivation plays a central role in development of non-small-cell lung cancer, then the frequency of gene inactivation in primary tumors should parallel that observed in cell lines.
Immunohistochemical staining was used to measure the expression of (wild‑type p53 induced phosphatase 1) Wip1, p38 mitogen‑activated protein kinase (MAPK), p53, p16 protein in a group of 60 NSCLC and 20 normal lung tissues.
In conclusion, our results indicate that p16 alterations constitute a major molecular abnormality in NSCLC with a considerable prognosis impact, promoter methylation being an important mechanism involved in p16 silencing.
In conclusion, the hypermethylation of the p16 and Wif-1 genes has potential as biomarkers that may be used to predict the prognosis of stage IA NSCLC.
It was the aim of this study to assess the expression of bmi-1 in resectable non-small cell lung cancer (NSCLC) in association with p16 and p14ARF (=human p19ARF).
Loss of p16 expression is a common event in NSCLC (232/365, 64%), especially in squamous cell carcinomas (97/115, 84%) in contrast to adenocarcinomas (93/186, 50%).
Methylation techniques have shown that these epigenetic changes commonly occur at the same frequency in numerous genes, both well-known ( FHIT, APC, p16 ) and recently discovered ( TMS1, RASSF1 ) in non-small cell lung cancer and in breast cancer.
Mutation at p16 occurred more frequently in non-small cell lung cancer (19.3%) than in small cell lung cancer (5.4%); while the mutation rate of Rb was 32.4% in small cell lung cancer versus 2.3% in non-small cell lung cancer.
Next-generation sequencing (NGS) for <i>TP53, RB1, STK11,</i> and <i>KEAP1</i> genes, as well as IHC for RB1 and P16 was performed on 79 and 109 cases, respectively, and correlated with overall survival (OS) and progression-free survival (PFS), stratifying for non-small cell lung cancer type chemotherapy including platinum + gemcitabine or taxanes (NSCLC-GEM/TAX) and platinum-etoposide (SCLC-PE).<b>Results:</b><i>RB1</i> mutation and protein loss were detected in 47% (<i>n</i> = 37) and 72% (<i>n</i> = 78) of the cases, respectively.
One hundred and fifty specimens from cancerous and adjacent non-cancerous tissue, bronchial washings and sputum from patients and 48 specimens, mostly sputum, from disease-free smokers were included. p16 methylation was very frequent in biopsies (82.85%) and bronchial washings (non-small cell lung carcinoma, 80.35%; small cell lung carcinoma, 16.66%) from patients, but also in adjacent non-cancerous tissue (45.71%).