Our findings did not show any correlation between promoter methylation of p73 and the other genes under study with clinicopathological parameters, including human papillomavirus infection and stage of the disease.
We characterised our in vitro panel extensively, with the aim to identify predictive factors for gefitinib effectiveness; all cell lines were free ofhuman papillomavirus infection, two were positive for Fhit expression, four expressed wild-type p53, and all of them variously expressed the other two p53 family members, p63 and p73.
These data support previous studies suggesting a role for HPV infection in OSCC and also indicate that HPV infection and p53 and p73 overexpression are not mutually exclusive.