Our current research activities focus on the biology of human epithelial tissues, particularly the epidermis and mucosa, which protect the organism from a hostile environment. As such, we seek to understand gene-environment interactions, including their effects on individuals and their impact on public health.
This research comprises three main areas: 1) directed differentiation of induced pluripotent stem cells into organoids for disease phenotype discovery; 2) studies of intrinsic and environmental stressors of the human epidermis including HPV infection, oncogenic stimuli, metabolic deregulation and radiation; and 3) squamous cell carcinoma and breast cancer development and progression.
In addition to the use of established systems, we have developed and published personalized human models. These include primary patient skin and tumor specimens, as well as derivative cell populations, 3-D spheres and engineered tissues. Genomic, transcriptomic, metabolomic and mechanistic exploration of these systems aims to discover disease drivers and biomarkers. Data obtained are then validated in human cohorts, xenografts and/or genetic mouse models. Our long-term goal is to identify cellular and viral determinants of cancer and to explore their targeting for the purpose of new interventions.
While fundamental basic knowledge discovery remains an important component of our program, we have made key transitions into the realm of translation. Research findings are thus routinely advanced by collaborating clinical teams at Cincinnati Children’s Hospital, the University of Cincinnati, and other national and international Institutions.
Experimental Hematology and Cancer Biology, Oncology, Cancer and Blood Diseases
Cancer Cell Metabolism: Implications for X-ray and Particle Radiation Therapy. International Journal of Particle Therapy. 2019; 5:40-48.
Limited detection of human polyomaviruses in Fanconi anemia related squamous cell carcinoma. PloS one. 2018; 13:e0209235.
Lipidomic Profiling Links the Fanconi Anemia Pathway to Glycosphingolipid Metabolism in Head and Neck Cancer Cells. Clinical Cancer Research. 2018; 24:2700-2709.
Dek overexpression in murine epithelia increases overt esophageal squamous cell carcinoma incidence. PLoS Genetics. 2018; 14:e1007227.
Risk of Human Papillomavirus Infection in Cancer-Prone Individuals: What We Know. Viruses-Basel. 2018; 10:E47.
The nuclear DEK interactome supports multi-functionality. Proteins: Structure, Function, and Bioinformatics. 2018; 86:88-97.
Overexpression of the human DEK oncogene reprograms cellular metabolism and promotes glycolysis. PloS one. 2017; 12:e0177952.
DEK associates with tumor stage and outcome in HPV16 positive oropharyngeal squamous cell carcinoma. Oncotarget. 2017; 8:23414-23426.
DEK is required for homologous recombination repair of DNA breaks. Scientific Reports. 2017; 7:44662.
Overcoming Pluripotent Stem Cell Dependence on the Repair of Endogenous DNA Damage. Stem Cell Reports. 2016; 6:44-54.
Susanne Wells, PhD4/11/2023
Susanne Wells, PhD9/6/2022
Susanne Wells, PhD11/23/2020