The goal of this study was to analyse alterations to p16 in squamous cell carcinoma (SCC) of the head and neck and to correlate these with clinical outcome.
We performed Western blotting and immunohistochemical analysis on tissues from 35 primary oral and laryngeal squamous carcinoma specimens with previous molecular analysis of the p16 gene and correlated the results with relevant clinicopathologic factors.
Both the adenocarcinoma and squamous cell carcinoma components revealed an inverse correlation between the expression pattern of p16 and RB proteins (p < 0.05).
To examine the role of DNA methylation as an explanation for these findings, we analyzed the DNA methylation patterns of the p16 INK4A promoter in DNA isolated from primary cultures of normal human oral keratinocytes and squamous cell carcinoma (SCC-15) oral cancer cells using bisulfite genomic sequencing.
Rb gene inactivation, reflected by the absence of Rb protein expression, has been reported in oral squamous cell carcinomas. p16INK4A is frequently deleted, methylated, or mutated, and cyclin D1 gene amplification in many malignancies including oral squamous cell carcinomas (SCC).
We studied p16 expression status by immunohistochemistry and telomerase activity using the TRAP assay in 21 premalignant lesions of the head and neck epithelium as well as 27 squamous-cell carcinomas.
To investigate the possibility that CDKN2A may be involved in the inherited susceptibility to SCCHN, the 3 coding exons of CDKN2A were sequenced in 40 patients who had developed a second primary cancer after an index squamous cell cancer of the head and neck.
The aim of this study was to determine p16INK4a point mutations and promoter hypermethylation in tumour cells and bronchial preneoplastic lesions in 32 surgically resected lungs due to primary squamous cell carcinoma.
Our analysis demonstrates that the mutations of the MTS1 locus in oral SCC specifically target expression of the p16(ink4a) gene but less frequently affect p14(ARF).
Co-incident methylation, accompanied by loss of expression, of sigma and p16INK4a was commonly detected in both SCC and VIN III, suggesting that epigenetic silencing of these two genes is an early and important event in vulval neoplasia.
Genetic status of cell cycle regulators in squamous cell carcinoma of the oesophagus: the CDKN2A (p16(INK4a) and p14(ARF) ) and p53 genes are major targets for inactivation.