M. L. Bristol

Fibroblast Stromal Support Model for Predicting Human Papillomavirus-Associated Cancer Drug Responses.

This paper develops a fibroblast co-culture model to predict drug responses in HPV+ cancers and shows it better predicts in vivo outcomes than in vitro alone.

Human Papillomavirus 16 replication converts SAMHD1 into a homologous recombination factor and promotes its recruitment to replicating viral DNA

This paper shows HPV16 replication converts SAMHD1 into a homologous recombination factor by phosphorylation, enhancing its recruitment to viral DNA and reducing replication.

Direct interaction with the BRD4 carboxyl-terminal motif (CTM) and TopBP1 is required for human papillomavirus 16 E2 association with mitotic chromatin and plasmid segregation function

This study shows that E2 protein interaction with BRD4's CTM and TopBP1 is essential for HPV16's mitotic chromatin association and plasmid segregation, offering therapeutic targets for viral genome targeting.

Human papillomavirus 16 E2 interaction with TopBP1 is required for E2 and viral genome stability during the viral life cycle.

This paper shows that HPV16 and HPV11 E2 proteins require interaction with TopBP1 for stability, and disrupting this interaction with CK2 inhibitors like CX4945 promotes viral genome integration and could be a therapeutic strategy.

Human papillomavirus 16 E2 repression of TWIST1 transcription is a potential mediator of HPV16 cancer outcomes

This paper shows that HPV16 E2 represses TWIST1 transcription, which may explain the better clinical outcomes in HPV16 positive cancers.

Estrogen attenuates the growth of human papillomavirus positive epithelial cells

This paper shows estrogen reduces growth of HPV-positive epithelial cells through two mechanisms, suggesting it could be a therapeutic for HPV+HNSCC.