In FY 2019, we investigated how HPV integration could result in de novo super-enhancer formation in cervical cancer. We characterized the chromatin and genomic landscape of a super-enhancer associated HPV integration site using whole genome sequencing, RNAseq, ChIPseq and molecular combing/fiber-FISH. Targeted disruption of factors binding to this element decreases viral transcription and causes cell death. Thus, cancer cells harboring integrated HPV may be targeted by therapeutics that disrupt super-enhancer function.
| McBride, Alison A; Münger, Karl (2018) Expert Views on HPV Infection. Viruses 10: |
| Warburton, Alix; Redmond, Catherine J; Dooley, Katharine E et al. (2018) HPV integration hijacks and multimerizes a cellular enhancer to generate a viral-cellular super-enhancer that drives high viral oncogene expression. PLoS Genet 14:e1007179 |
| McBride, Alison A (2017) Oncogenic human papillomaviruses. Philos Trans R Soc Lond B Biol Sci 372: |
| McBride, Alison A (2017) Playing with fire: consequences of human papillomavirus DNA replication adjacent to genetically unstable regions of host chromatin. Curr Opin Virol 26:63-68 |
| McBride, Alison A; Warburton, Alix (2017) The role of integration in oncogenic progression of HPV-associated cancers. PLoS Pathog 13:e1006211 |
| Dooley, Katharine E; Warburton, Alix; McBride, Alison A (2016) Tandemly Integrated HPV16 Can Form a Brd4-Dependent Super-Enhancer-Like Element That Drives Transcription of Viral Oncogenes. MBio 7: |
