Breast cancer is the most frequently diagnosed cancer and the second-leading cause of cancer-associated deaths in women. There is a multitude of risk factors for breast cancer that women cannot change, such as a family history of breast cancer, getting older, genetic mutations and menstruation history. As such, researchers need to continue finding better ways to treat and prevent breast cancer.
I have a long-standing interest in genetics and genome stability, which is essential for protecting cells from transformation and eventual tumor development. This reason, combined with personal experiences of family members with cancer, led me to study the intersection of molecular genetics and cancer biology.
My research areas involve finding the molecular and cellular drivers of mammary gland development and breast cancer progression. For instance, my laboratory concentrates on the DEK oncogene and how it functions in DNA repair and transcription.
We look at how the DEK oncogene leads to hyperplasia and tumorigenesis. Our work, in collaboration with others, was the first to recognize DEK as a commonly over-expressed oncogenic driver of breast cancer.
The general goal of my team is to determine how problems in expressing the chromatin-binding DEK protein leads to cellular and molecular pathogenesis in human disease. Another goal we have in our lab is to streamline drug development in order to find new treatments to remedy solid tumors.
Other projects my team and I work on include:
Throughout my career, I have garnered multiple recognitions, including:
I have more than 15 years of experience in cancer research, and I first started working at Cincinnati Children’s Hospital Medical Center in 2008. My research has been published in numerous journals, including Schizophrenia Research, Cancer Research, Nature Communications and Translational Oncology. I am an active member in both the American Association for Cancer Research (AACR) and the Society for Experimental Biology.
In addition to my research program, I’m the Director of the Office of Postdoctoral Affairs at Cincinnati Children’s. For more information about postdoctoral research fellowship positions at Cincinnati Children’s, visit the Office of Postdoctoral Affairs webpage.
BA: Miami University, Oxford, OH, 2002.
MS: University of Michigan, Ann Arbor, MI, 2004.
PhD: University of Michigan, Ann Arbor, MI, 2008.Postdoctoral Fellowship: Cincinnati Children's Medical Center, Cincinnati, OH, 2012.
Breast cancer; gene expression; metastasis; cell cycle; DEK; oncogenes and tumor suppressors
Oncology, Cancer and Blood Diseases
Drug resistance mechanisms create targetable proteostatic vulnerabilities in Her2+ breast cancers. PLoS ONE. 2022; 17.
Novel molecular mechanisms in Alzheimer's disease: The potential role of DEK in disease pathogenesis. Frontiers in Aging Neuroscience. 2022; 14.
In silico gene expression and pathway analysis of DEK in the human brain across the lifespan. European Journal of Neuroscience. 2022; 56:4720-4743.
Inhibition of the RacGEF VAV3 by the small molecule IODVA1 impedes RAC signaling and overcomes resistance to tyrosine kinase inhibition in acute lymphoblastic leukemia. Leukemia. 2022; 36:637-647.
Defective transcription elongation in human cancers imposes targetable proteotoxic vulnerability. Translational Oncology. 2022; 16.
Loss of DEK Expression Induces Alzheimer's Disease Phenotypes in Differentiated SH-SY5Y Cells. Frontiers in Molecular Neuroscience. 2020; 13.
DEK Expression in Breast Cancer Cells Leads to the Alternative Activation of Tumor Associated Macrophages. Cancers. 2020; 12.
IODVA1, a guanidinobenzimidazole derivative, targets Rac activity and Ras-driven cancer models. PLoS ONE. 2020; 15.
The Small Molecule IODVA1 Inhibits the Rac Guanine Nucleotide Exchange Factor Vav3 and Overcomes TKI-Resistance in Ph+(BCR-ABL1) B-ALL. Blood. 2019; 134:4647-4647.
Optical Redox Imaging Detects the Effects of DEK Oncogene Knockdown on the Redox State of MDA-MB-231 Breast Cancer Cells. Molecular Imaging and Biology. 2019; 21:410-416.