Are there differences in the staining pattern of p16INK4a in dysplastic or neoplastic cells where the HPV genome is episomal in contrast to cells where the HPV-DNA is integrated into the chromosomal DNA of the host cells?
There is no evidence for differences in p16INK4a staining patterns in relation to the episomal as opposed to the integrated forms of HPV-DNA up to now. In the cause of HPV-related carcinogenesis, disturbances of the spindle pole apparatus in proliferating cells are a well-known phenomenon. This is considered to be a strong promoter for chromosomal breakage and recombination leading to integration of episomal viral DNA into the host genome. p16INK4a over-expression, however, should be detected regardless whether the HPV genome is integrated or episomal.
