Associate Professor

Areas of Interest
Environmental exposures, electronic cigarettes, endocrine disrupting compounds, dietary and lifestyle exposures, DNA damage and repair, transcriptional modulation of DNA repair, cellular response to chemotherapeutics, predictive biomarkers, and biological drivers of health disparities.



I received a BA in chemistry from Michigan State University. I earned a Ph.D. from the University of California Los Angeles in Chemistry. I studied single-molecule fluorescence and bacterial transcription initiation in the laboratory of Dr. Shimon Weiss. My postdoctoral training started at Wake Forest University School of Medicine in cancer biology and was completed at
the National Institute of Environmental Health Sciences. In the laboratory of Dr. Samuel H. Wilson, I examined the role of DNA repair in response to environmental exposures and how modulated DNA repair machinery contributed to genotoxicity and carcinogenesis.

  • Research Interests

    As an associate professor of pharmacology and toxicology at the University of Alabama at Birmingham with joint appointments in Nutrition Sciences and at the O’Neal Comprehensive Cancer Center, my work focuses on characterizing the influence environmental exposures have on DNA damage and repair. We have three major research areas focused on this goal. RADD- Repair Assisted Damage Detection My lab has developed an easy-to-use, flexible DNA damage measurement assay, Repair Assisted Damage Detection (RADD). RADD is a versatile detection method to identify deficiencies in repair mechanisms. Using DNA repair enzymes, we can label sites of DNA damage in isolated DNA, cells, and tissues to understand the DNA damage landscape. We use this method with our expertise in environmental exposures to understand the types of DNA damage that result from exposures, to identify defective DNA repair machinery allowing DNA damage to persist within the genome, and to map interactions between proteins, cells and tissues that promote DNA repair dysfunction or altered DNA repair profiles. Understanding cellular consequences of dihydroxyacetone exposures Dihydroxyacetone (DHA) is the active ingredient in sunless tanning products and is produced as a combustion product by electronic cigarettes (e-cigarettes). Once inhaled or absorbed, DHA rapidly enters the bloodstream and is quickly transported into cells. DHA is then converted into its phosphorylated form, dihydroxyacetone phosphate (DHAP), entering multiple metabolic pathways. We have been characterizing the cytotoxicity and genotoxicity of DHA to better understand its exposure effects for e-cigarette users. DHA is cytotoxic across several cell line models, and its effects are highly cell-type specific. DHA is a unique product in e-cigarettes not found in traditional cigarettes. We aim to understand inhalation and systemic exposures to this agent and its relevant e-cigarette aerosol mixtures. E-cigarettes may pose additional health risks from these novel combustion products, and it is critical we understand the exposure risks to these toxins and toxicants. Base excision repair defects and their influence on therapeutic evasion Using RADD and other techniques, we are also examining changes in the expression of key base excision repair proteins in breast, prostate, and other cancers. Mutations in DNA repair proteins and their loss of function have been highly focused on in cancer. Yet, changes in expression levels of these proteins can also cause detrimental effects, including genomic instability. Environmental exposures and endogenous metabolic changes induce these changes, dysregulating DNA repair pathways, promoting mutations and genomic instability leading to cancer. In cancer, dysregulated DNA repair pathways can also drive cancer aggressiveness and resistance to DNA-damaging therapies. Therefore, understanding how exposures or changes in metabolic processes drive expression changes in DNA repair proteins may offer new insight into cancer development. More importantly, it could offer new insight into biological drivers in health disparities and new opportunities for molecular targeting in cancer drug development. With this suite of research projects, our long-term goal is to understand how voluntary and involuntary exposures alter a cell’s DNA repair ability and how these changes result in cancer. By mapping DNA damage and repair changes, we hope to inform new clinical biomarkers or identify new molecular targets to improve therapeutic choice and therapy outcomes for cancer patients.

  • Selected Publications

    Wright G, Gassman N. Glucose Increases STAT3 Activation, Promoting Sustained XRCC1 Expression and Increasing DNA Repair. International Journal of Molecular Sciences. 2022 April 13; 23(8):4314-. Available from: DOI: 10.3390/ijms23084314

    Krieger K, Gohlke J, Lee K, Piyarathna D, Castro P, Jones J, Ittmann M, Gassman N, Sreekumar A. Repair-Assisted Damage Detection Reveals Biological Disparities in Prostate Cancer between African Americans and European Americans. Cancers. 2022 February 17; 14(4):1012-. Available from: DOI: 10.3390/cancers14041012

    Wright G, Sonavane M, Gassman N. Activated STAT3 Is a Novel Regulator of the XRCC1 Promoter and Selectively Increases XRCC1 Protein Levels in Triple Negative Breast Cancer. International Journal of Molecular Sciences. 2021 May 22; 22(11):5475-. Available from: DOI: 10.3390/ijms22115475

    Mann E, Lee K, Chen D, da Silva L, Dal Zotto V, Scalici J, Gassman N. Associations between DNA Damage and PD-L1 Expression in Ovarian Cancer, a Potential Biomarker for Clinical Response. Biology. 2021 April 29; 10(5):385-. Available from: DOI: 10.3390/biology10050385

    Lee KJ, Wright G, Bryant H, Wiggins L, Schuler M, Gassman NR. EGFR signaling promotes resistance to CHK1 inhibitor prexasertib in triple negative breast cancer. Cancer Drug Resistance. 2020 December 05; 3(4):980-991. Available from: 10.20517/cdr.2020.73

    Wright G, Gassman NR. Transcriptional dysregulation of base excision repair proteins in breast cancer. DNA Repair (Amst). 2020 Sep;93:102922. PubMed PMID: 33087263.

    Lee KJ, Mann E, Wright G, Piett CG, Nagel ZD, Gassman NR. Exploiting DNA repair defects in triple negative breast cancer to improve cell killing. Ther Adv Med Oncol. 2020;12:1758835920958354. PubMed Central PMCID: PMC7502856.

    Lee KJ, Mann E, da Silva LM, Scalici J, Gassman NR. DNA damage measurements within tissue samples with Repair Assisted Damage Detection (RADD). Curr Res Biotechnol. 2019 Nov;1:78-86. PubMed Central PMCID: PMC8118132.

    Torchinsky D, Michaeli Y, Gassman NR, Ebenstein Y. Simultaneous detection of multiple DNA damage types by multi-colour fluorescent labelling. Chem Commun (Camb). 2019 Sep 19;55(76):11414-11417. PubMed Central PMCID: PMC6783632.

    Lee KJ, Piett CG, Andrews JF, Mann E, Nagel ZD, Gassman NR. Defective base excision repair in the response to DNA damaging agents in triple negative breast cancer. PLoS One. 2019;14(10):e0223725. PubMed Central PMCID: PMC6785058.

    Smith KR, Hayat F, Andrews JF, Migaud ME, Gassman NR. Dihydroxyacetone Exposure Alters NAD(P)H and Induces Mitochondrial Stress and Autophagy in HEK293T Cells. Chem Res Toxicol. 2019 Aug 19;32(8):1722-1731. PubMed Central PMCID: PMC6701868.

    Daniel CL, Gassman NR. A truly safer alternative? Sunless tanning products and the unknown. Prev Med. 2018 Jul;112:45-46. PubMed PMID: 29626559.

    Holton N, Ebenstein Y, Gassman N. Broad spectrum detection of DNA damage by Repair Assisted Damage Detection (RADD). DNA Repair. 2018 June; 66-67:42-49. Available from: DOI: 10.1016/j.dnarep.2018.04.007

    Smith KR, Granberry M, Tan MCB, Daniel CL, Gassman NR. Dihydroxyacetone induces G2/M arrest and apoptotic cell death in A375P melanoma cells. Environ Toxicol. 2018 Mar;33(3):333-342. PubMed Central PMCID: PMC5809210.

    Tan MCB, Gassman NR, Fernandez AM, Bae S, Daniel CL. High prevalence of combination tanning among undergraduates: Survey at a southeastern US university. J Am Acad Dermatol. 2017 Nov;77(5):968-970. PubMed PMID: 29029906.


Ph.D., Department of Chemistry, University of California, Los AngelesPostdoctoral Fellowships

Postdoctoral Fellowships
Postdoctoral Fellow, Wake Forest School of Medicine
Postdoctoral Fellow, National Institute of Environmental Health SciencesContact

Office Location
Volker Hall 156