Cervical cancer is one of the leading causes of cancer death in women worldwide. 
Human papillomavirus (HPV) infection is necessary but not sufficient for the 
development of cervical cancer. Genomic instability caused by HPV allows cells 
to acquire additional mutations required for malignant transformation. Genomic 
instability in the form of polyploidy has been implicated in a causal role in 
cervical carcinogenesis. Polyploidy not only occurs as an early event during 
cervical carcinogenesis but also predisposes cervical cells to aneuploidy, an 
important hallmark of human cancers. Cell cycle progression is regulated at 
several checkpoints whose defects contribute to genomic instability.The 
high-risk HPVs encode two oncogenes, E6 and E7, which are essential for cellular 
transformation in HPV-positive cells. The ability of high-risk HPV E6 and E7 
protein to promote the degradation of p53 and pRb, respectively, has been 
suggested as a mechanism by which HPV oncogenes induce cellular transformation. 
E6 and E7 abrogate cell cycle checkpoints and induce genomic instability that 
leads to malignant conversion.Although the prophylactic HPV vaccine has recently 
become available, it will not be effective for immunosuppressed individuals or 
those who are already infected. Therefore, understanding the molecular basis for 
HPV-associated cancers is still clinically relevant. Studies on genomic 
instability will shed light on mechanisms by which HPV induces cancer and hold 
promise for the identification of targets for drug development.