Nicholas Wallace, Associate Professor

Nick Wallace

Contact information

266 Chalmers Hall
nwallac@ksu.edu

Lab website: http://wallacelabksu.weebly.com

Education

Ph.D. 2008, Tulane University. Biochemistry.

Area(s) of specialization

Human Papillomavirus; Viral Oncogenesis; DNA Damage Repair

Research Focus

The Wallace Lab offers excellent training opportunities for undergraduate, post-baccalaureate (as lab technicians), graduate, and post-doctoral trainees interested in biomedical research. Trainees have exceptional productivity. All post-baccalaureate fellows become published authors. Undergraduates have won prestigious awards (e.g., Goldwater Fellowship) and all become published authors. Graduate students have produced 4-5 first-author papers (8 papers total) in high impact journals, earning doctorates in ~5 years. All post-doctoral fellows have received external funding and are given abundant mentoring opportunities that prepare them for future leadership positions. Lab members perfect standard molecular biology techniques and acquire highly marketable skills (e.g., live cell microscopy and single cell sequencing). Further, trainees participate in national and international (D.C., Canada, United Kingdom, Italy) conferences. As a result, Wallace lab alumni have gone on to careers in industry with leading companies (e.g., Eli Lilly and Enliven Therapeutics) and in academia with elite institutions (e.g., St. Jude Children’s Research Hospital, MD Anderson Cancer Center, Fred Hutchinson Cancer Research Center).

Our work focuses on 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). HPVs do not encode their own replicative machinery and must hijack polymerases from their host cell. Thus, they are dependent on continually cycling cells for their own replication. To avoid the cell cycle arrest that accompanies DNA damage, these viruses express oncoproteins (HPV E6 and E7) that dysregulate the cell cycle. HPV E6 and E7 accomplish this deregulation directly by degrading checkpoint proteins and indirectly by attenuating host DNA repair.

We characterize the repair deficiencies caused by HPV oncogenes, from two HPV genera with two distinct goals. We are looking to exploit the deficiencies caused high risk alpha HPV oncogenes (cause cervical and many other cancers) to improve care for the tumors caused by these viruses. We are also interested in the beta genus of HPVs. These viruses are hypothesized to act as a co-factor in cutaneous malignancies by promoting genome destabilization. We study beta HPV biology to assess their hypothesized transformative properties.

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. https://doi.org/10.3390/cancers13010028.

Dacus D, Cotton C, McCallister TX, Wallace NA. Beta Human Papillomavirus 8E6 Attenuates LATS Phosphorylation after Failed Cytokinesis. J Virol 2020;94:. https://doi.org/10.1128/JVI.02184-19.

Wallace NA. Catching HPV in the Homologous Recombination Cookie Jar. Trends Microbiol 2020;28:191–201. https://doi.org/10.1016/j.tim.2019.10.008.

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:. https://doi.org/10.3390/cancers12092356.

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. https://doi.org/10.1016/j.virol.2020.07.004.

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. https://doi.org/10.1016/j.virol.2020.07.016.

Wallace NA. mSphere of Influence: the Value of Simplicity in Experiments and Solidarity among Lab Members. MSphere 2019;4:. https://doi.org/10.1128/mSphere.00172-19.

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:. https://doi.org/10.3390/pathogens8040267.

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. https://doi.org/10.1016/j.gene.2018.11.079.

View the complete publication list in NCBI