Nicholas Wallace, Associate Professor

Nick Wallace

Contact information

266 Chalmers Hall

Lab website:


Ph.D. 2008, Tulane University. Biochemistry.

Area(s) of specialization

Human Papillomavirus; Viral Oncogenesis; DNA Damage Repair

Research Focus

Infectious agents cause up to 20% of all human cancers. These oncogenic pathogens include the Human Papillomaviruses (HPVs) that cause cancers of the anogenital and oropharyngeal tracts and may also contribute to the development of non-melanoma skin cancers (NMSC). A cancer caused by these lethal viruses will kill at least 1 woman in the time it takes to read this summary of our work.

HPVs do not encode their own replicative machinery and must hijack polymerases from their host cell. As a result, they are dependent on continually cycling cells for their own replication. To avoid the cell cycle arrest that accompanies DNA damage repair, these viruses express oncoproteins (HPV E6 and E7) that disrupt cell cycle regulation. HPV E6 and E7 accomplish this deregulation both directly by promoting the degradation of cell cycle regulatory proteins and indirectly by attenuating host DNA damage repair. To avoid propagating errors, in response to genomic insults, cells pause their progression through the cell cycle until the lesion is fixed. By diminishing the cell's ability to respond to damage, the virus maintains access to the replicative machinery need for its own life cycle by sacrificing the cell's genomic integrity.

Our lab characterizes the repair deficiencies caused by HPV oncogenes, from two HPV genera with two distinct goals. First, we study the repair deficiencies caused by oncogenes from high risk members of the Alpha Genus (viruses that are the causative agent in cervical and many other cancers), in order to predict novel chemotherapeutic targets for the tumors associated with these viral infections. We are also interested in the Beta genus of HPVs. These viruses are hypothesized to act as a co-factor in non-melanoma skin cancers by inhibiting repair of UV damage. This hypothesis is evaluated in our lab by characterizing the repair of DNA lesions in cells expressing Beta HPV oncogenes.

Selected Publications

Wendel SO, Snow JA, Bastian T, Brown L, Hernandez C, Burghardt E, et al. High Risk α-HPV E6 Impairs Translesion Synthesis by Blocking POLη Induction. Cancers 2021;13:28.
Dacus D, Cotton C, McCallister TX, Wallace NA. Beta Human Papillomavirus 8E6 Attenuates LATS Phosphorylation after Failed Cytokinesis. J Virol 2020;94:.
Wallace NA. Catching HPV in the Homologous Recombination Cookie Jar. Trends Microbiol 2020;28:191–201.
Hu C, Bugbee T, Gamez M, Wallace NA. Beta Human Papillomavirus 8E6 Attenuates Non-Homologous End Joining by Hindering DNA-PKcs Activity. Cancers 2020;12:.
Holcomb AJ, Brown L, Tawfik O, Madan R, Shnayder Y, Thomas SM, et al. DNA repair gene expression is increased in HPV positive head and neck squamous cell carcinomas. Virology 2020;548:174–81.
Dacus D, Riforgiate E, Wallace NA. β-HPV 8E6 combined with TERT expression promotes long-term proliferation and genome instability after cytokinesis failure. Virology 2020;549:32–8.
Wallace NA. mSphere of Influence: the Value of Simplicity in Experiments and Solidarity among Lab Members. MSphere 2019;4:.
Snow JA, Murthy V, Dacus D, Hu C, Wallace NA. β-HPV 8E6 Attenuates ATM and ATR Signaling in Response to UV Damage. Pathog Basel Switz 2019;8:.
Gu W, Sun S, Kahn A, Dacus D, Wendel SO, McMillan N, et al. Cervical cancer cell lines are sensitive to sub-erythemal UV exposure. Gene 2019;688:44–53.

View the complete publication list in NCBI