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BACKGROUND Epigenetic modifications in host cells, like  p16    ink4a   methylation, have been considered as putative complementary mechanisms for cancer development. Because only a small proportion of infected women develop cervical cancer, other factors might be involved in carcinogenesis, either independently or in association with high-risk human papillomavirus (HR-HPV) infections, including epigenetic factors. OBJECTIVES We hypothesised that  p16    ink4a   methylation might have a role in cancer development driven by HPV16, mainly in the presence of intact  E1/E2  genes. Thus, our objectives were to assess the status of  p16    ink4a   methylation and the HPV16  E1/E2  integrity in samples in different stages of cervical diseases. METHODS Presence of HPV16 was determined by E6 type-specific polymerase chain reaction (PCR). Methylation status of the  p16    ink4a   promoter was assessed by methylation-specific PCR in 87 cervical specimens comprising 29 low-grade (LSIL), 41 high-grade (HSIL) lesions, and 17 cervical cancers (CC). Characterisation of E1 and E2 disruption (as an indirect indicator of the presence of episomal viral DNA) was performed by PCR amplifications. FINDINGS We observed a significantly increased trend ( nptrend  = 0.0320) in the proportion of methylated  p16    ink4a   in cervical samples during cancer development. Concomitant  E1  and  E2  disruptions were the most frequent pattern found in all groups: CC (76%), HSIL (54%), and LSIL (73%). No statistically significant differences between  p16    ink4a   methylation and  E1/E2  integrity, in histological groups, was observed. MAIN CONCLUSIONS There was an increase in methylation of the  p16    ink4a   promoter from pre-neoplastic lesions to cancer. Additionally, a high frequency of  E1/E2  disruptions in LSIL/HSIL suggested that viral DNA integration was an early event in cervical disease. Moreover, the methylation status was apparently independent of HPV16 integrity.

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Methylation of p16 ink4a promoter is independent of human papillomavirus DNA physical state: a comparison between cervical pre-neoplastic and neoplastic samples