Five percent of all human cancers are caused by infections with human papillomaviruses (HPVs). While previous research has focused on the protein targets of E6 and E7 (most extensively the tumor suppressors p53 and RB1), the majority of the human transcriptome does not encode proteins. In the Munger lab we are interested in determining how long noncoding RNAs are involved in HPV pathogenesis and carcinogenesis. We have previously shown that E6 and E7 dysregulate the expression of over 1000 lncRNAs. I am particularly interested in lncRNAs that mediate p53 activities and/or function as upstream regulators of p53. This is because cervical carcinoma cells maintain wild-type p53, and by targeting lncRNAs expression we can potentially restore p53 function as a therapeutic modality.