Member of: The Karl Munger Lab
Human papillomaviruses (HPVs), a group of non-enveloped, double-stranded DNA viruses, cause five percent of all cancers worldwide. Given that the high-risk HPV E6 and E7 oncoproteins contribute to nearly every cancer hallmark, the Munger Lab is interested in identifying specific vulnerabilities in HPV-positive cancers that could be therapeutically targeted. My research focuses on the role of E7 in binding and degrading the pRB tumor suppressor, thereby allowing infected cells to evade growth suppression. Efforts to develop therapeutic approaches to restore tumor suppressor activity have been largely unsuccessful, so I am interested in finding druggable modifier genes of tumor suppressor pathways.
BS, Biology, University of Massachusetts - Amherst, Amherst, MA