Nikki Lytle, PhD

Nikki K. Lytle, PhD

Assistant Professor


  • TBRC, C4783

Contact Information

General Interests

Cell state plasticity, tumor evolution, tumor microenvironment, pancreatic cancer, breast cancer


PhD, Biomedical Sciences, University of California San Diego, 2018


Dr. Lytle completed her graduate work at the University of California San Diego in Dr. Tannishtha Reya’s lab where she focused on identifying signals that are critical for pancreatic cancer initiation, therapy-resistance, and metastasis. Her work contributed to important therapeutically-relevant discoveries including the identification of Musashi as a pancreatic cancer stem cell determinant, and disabling pancreatic cancer progression through blockade of the stem cell regulators ROR-gamma and LIF. She then went on to join Dr. Geoffrey Wahl’s lab at the Salk Institute for her postdoctoral fellowship where she studied how tissue injury can contribute to cell state instability and tumor initiation in breast cancer, or progression to metastasis in pancreatic cancer. Dr. Lytle was named a Hope Funds for Cancer Research Fellow in 2019 for her work in pancreatic cancer. She joined the Department of Surgery at the Medical College of Wisconsin in 2022. Her current research program focuses on cell intrinsic and microenvironmental factors that contribute to pancreatic and breast cancer with the goal of identifying novel therapeutic targets for preventing metastatic progression.

Research Interests

Our understanding of cancer has been challenged in nearly every regard. “Potent” oncogenic mutations are insufficient to drive tumorigenesis from most cells. What factors are required to initiate cancer? Do rare tumor-initiating cells have an inherent “permissive” epigenetic state, or is tumor-initiating potential determined by local signals from the microenvironment? Additionally, tumor cells spread throughout the body early in disease, some with mesenchymal characteristics and others stuck in an epithelial state, suggesting that the route to metastasis may be heterogeneous and complicated. The vast majority of these disseminated cells will die or be cleared by our immune system and only a select few drive metastasis. What properties endow those rare cells to survive and initiate metastases?

My research focuses on understanding cell states that are responsible for tumor initiation, therapy resistance and metastasis. We study human conditions in which cancer progression is either diminished or enhanced as a platform for determining anti- or pro-tumorigenic signals, respectively. We leverage patient samples as the primary source of discovery, and employ multiplexed single cell analyses of tumor and microenvironmental cell populations to identify signals that critically contribute to metastasis or therapy resistance. We utilize elegant mouse models that enable tracking of cell dynamics over time and functional testing of targets, and work to develop new tools to address outstanding questions in cancer biology when current tools are inadequate. Finally, we focus on targets that may be therapeutically actionable with the goal of moving our findings into the clinic to improve patient outcomes.