Michelle Ng

Human papillomaviruses (HPVs) play a causative role in cervical cancer. Integration of viral DNA into the host genome occurs in >80% of cases, but the resulting disruption of genome structure and function is poorly understood. We hypothesize that HPV integrations disrupt the 3D organization of the host genome, leading to regulatory rewiring and aberrant activation of oncogenic programs. By relating genome topology with other types of ‘omic data in HPV+ cervical cancer cell lines and patient samples, we aim to better understand the dysregulation caused by HPV integrations, and how it influences cervical cancer pathogenesis. Findings in this context may improve our understanding of genome dysregulation in other HPV-associated cancers, and provide general insights into how viral integration can promote cancer progression.

Recent publications.