AIMS: A defective DNA damage response can result in genomic instability (GIN) 
and lead to transformation to cancer. As p53-binding protein 1 (53BP1) localizes 
at the sites of DNA double strand breaks (DSBs) and rapidly forms nuclear foci 
(NF), the presence of 53BP1 NF can be considered to be an indicator of 
endogenous DSBs reflecting GIN. Our aim was to analyse the presence of DSBs by 
immunofluorescence for 53BP1 expression in a series of cervical lesions, to 
evaluate the significance of GIN during carcinogenesis.
METHODS AND RESULTS: A total of 80 archival cervical tissue samples, including 
11 normal, 16 cervical intraepithelial neoplasia (CIN)1, 15 CIN2, 24 CIN3 and 14 
squamous cell carcinoma samples, were analysed for 53BP1 NF, human 
papillomavirus (HPV) infection, and p16(INK4a) overexpression. The number of 
53BP1 NF in cervical cells appeared to increase with progression during 
carcinogenesis. The distribution of 53BP1 NF was similar to that of the punctate 
HPV signals as determined by in-situ hybridization and also to p16(INK4a) 
overexpression in CIN, suggesting an association with viral infection and 
replication stress.
CONCLUSIONS: Immunofluorescence analysis of 53BP1 expression can be a useful 
tool with which to estimate the level of GIN. During cervical carcinogenesis, 
GIN may allow further accumulation of genomic alterations, causing progression 
to invasive cancer.