A total of 67 samples of tumor tissue from squamous cell carcinomas of the oral cavity, the pharynx and the larynx were analysed for an inactivation of p16.
This is the first description of specific abnormalities in tumor suppressor genes in RDEB associated SCC, and demonstrates that alterations in both p53 and p16ink4a can contribute to RDEB associated SCC.
Disrupted Rb pathway (loss of expression of RB1 and/or of CDKN2A) in 55.9% of analysed cases confirmed the hypothesis that RB1 pathway is altered in head and neck squamous cell carcinomas, with CDKN2A (45%), rather than RB1 (11.8%) being more frequently inactivated.
The aim of our study was to analyze the relationship between genetic changes leading to inactivation of the CDKN2A gene and subsequent alteration of protein expression in squamous cell cancer of the larynx (SCCL) in connection with the clinical and histopathological course of the disease.
It is concluded that p16 is frequently expressed in squamous carcinoma of the cervix, vagina and vulva, but not seen in cases of benign and low grade lesions.
Twenty percent of in situ squamous cell carcinomas had moderate to strong staining in only the lower half to lower two thirds of the epidermis, whereas 70% of the in situ squamous cell carcinomas exhibited full-thickness p16 staining, with no staining in the dermis.
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.
We explored the immunohistochemical expression of FAS, Ki-67 and p53 in squamous cell carcinomas (SCC) of the larynx and their association with clinicopathological features and outcome.
In a chemical genetics screen for small molecule activators of Notch signalling, we identified epidermal growth factor receptor (EGFR) as a key negative regulator of Notch1 gene expression in primary human keratinocytes, intact epidermis and skin squamous cell carcinomas (SCCs).