Map showing global impact of cervical cancer 2012

ICGEB studies open way for therapeutics to specifically block cervical cancer growth and invasion

A recent ground-breaking publication in PLoS Pathogens, a peer-reviewed, Open Access journal, from the Tumour Virology Laboratory shows that phosphorylation of the HPV E7 oncoprotein by a cellular kinase, CKII, is essential for tumour maintenance.

Human Papillomaviruses are the causative agents of cervical cancer, which remains a major cause of morbidity and death in many parts of the world with over 500,000 cases annually. Whilst there are now excellent vaccines against HPV, there are major limitations in delivery and uptake in many parts of the world where they are most needed. Improved therapies for cervical cancer are of the utmost urgency.

Strategy for genome editing: Validation of the genome editing with Sanger sequencing

By using state-of-the-art genome-editing approaches, the Group has found that blocking phosphorylation of E7 actually inhibits tumour cell growth and invasive potential. These studies therefore, open up the way for using specific inhibitors of CKII activity as novel therapeutics to specifically block cervical cancer growth and invasion.

Link to the Article: The HPV-18 E7 CKII phospho acceptor site is required for maintaining the transformed phenotype of cervical tumour-derived cells