I am a statistical geneticist, which means it is my job to make sense of the large volumes of genetic data being produced. My interest in genetics started with my first introduction to the field in high school. Because I was always good at math, I was excited to learn about statistical genetics, where I could marry my two interests.
Here at Cincinnati Children’s Hospital Medical Center, my primary focus is the genetic contributions to variation in phenotypes (characteristics of people). Rather than look at a single characteristic, I focus on many, including inappropriate heart development, allergic conditions (including asthma and eosinophilic esophagitis), and how people respond to medications.
My approach to variation in phenotypes is to consider multiple factors jointly. This is important because we often find that a single genetic variant does not explain outcomes. Rather, the context in which a gene variant occurs (other genetic variants, environmental factors) is important. My research focuses on identifying combinations of factors that best explain phenotypes. This work has resulted in a better understanding of heart development and why certain individuals develop asthma or eosinophilic esophagitis.
My role at Cincinnati Children’s extends beyond my research. I am proud to support the next generation of researchers and have mentored many students, trainees and faculty throughout my career.
BA: University of Kansas, Lawrence, KS, 1991.
MA: University of Kansas, Lawrence, KS, 1993.
PhD: (with Honors) University of Kansas, Lawrence, KS, 1999.
Post-doctoral fellow: Southwest Foundation for Biomedical Research, San Antonio, TX, 2002.
Statistical genetics; genetics of heart malformations; pharmacogenetics; genetics of allergic disorders
International Consensus Recommendations for Eosinophilic Gastrointestinal Disease Nomenclature. Clinical Gastroenterology and Hepatology. 2022; 20:2474-2484.e3.
Multiancestral polygenic risk score for pediatric asthma. Journal of Allergy and Clinical Immunology. 2022; 150:1086-1096.
The genetic architecture of pediatric cardiomyopathy. American Journal of Human Genetics. 2022; 109:282-298.
Novel role for caspase recruitment domain family member 14 and its genetic variant rs11652075 in skin filaggrin homeostasis. Journal of Allergy and Clinical Immunology. 2022; 149:708-717.
Desmoplakin and periplakin genetically and functionally contribute to eosinophilic esophagitis. Nature Communications. 2021; 12.
Sensitization to peanut, egg or pets is associated with skin barrier dysfunction in children with atopic dermatitis. Clinical and Experimental Allergy. 2021; 51:666-673.
CYP2D6 Phenotype Influences Aripiprazole Tolerability in Pediatric Patients with Mood Disorders. Journal of Child and Adolescent Psychopharmacology. 2021; 31:56-62.
Building a Population Representative Pediatric Biobank: Lessons Learned From the Greater Cincinnati Childhood Cohort. Frontiers in Public Health. 2021; 8.
Very early onset eosinophilic esophagitis is common, responds to standard therapy, and demonstrates enrichment for CAPN14 genetic variants. Journal of Allergy and Clinical Immunology. 2021; 147:244-254.e6.