Abstract

Cervical carcinoma is the third most common cause of cancer-related deaths in women worldwide. The full impact of vaccination against high-risk human papillomavirus (HRHPV) will not be seen for ~20 years and there will be no benefits for women who are already HRHPV positive. Current treatments for cervical carcinoma have not changed for decades and survival rates for advanced disease remain low.

Our group investigates key events in the development of cervical squamous cell carcinoma (SCC) following infection with HRHPV , using clinical samples and the W12 in vitro model system. We study mechanisms of viral persistence in cervical epithelial cells, causes of deregulated viral transcription in proliferating epithelium and the significance of common host genomic changes induced by over-expressed HRHPV oncogenes.

We recently identified that cervical keratinocytes containing HPV16 episomes show specific inhibition of responses to dsRNA through down-regulation of TLR3 and RIG -I receptors and that the oncostatin M receptor is commonly over-expressed in cervical carcinomas and contributes significantly to disease progression.