Gwen Lomberk, PhD

Gwen Lomberk, PhD

Chief, Division of Research; Director, Basic Science Research; Department of Surgery; Professor of Surgery and Pharmacology & Toxicology

Contact Information


PhD, Cancer Biology, Mayo Graduate School, 2002

Research Experience

  • Cell Cycle Proteins
  • Cell Nucleus Shape
  • Chromatin
  • Chromatin Assembly and Disassembly
  • Chromatin Immunoprecipitation
  • Chromosomal Proteins, Non-Histone
  • Epigenesis, Genetic
  • Gene Expression Regulation
  • Gene Expression Regulation, Neoplastic
  • Histone Code
  • Histone-Lysine N-Methyltransferase
  • Kruppel-Like Transcription Factors

Leadership Positions

  • Chief, Division of Research
  • Director Basic Science Research, Department of Surgery

Research Interests

Epigenomic-based pharmacology has the potential to serve as a robust tool to improve the future treatment of pancreatic cancer (PDAC), which is the focus of my research program. My laboratory seeks to contribute to the field of experimental therapeutics through combined inhibition of a genetic-to-epigenetic pathway to treat PDAC, as an important and provocative consideration for harnessing the capacity of cell cycle inhibitors in efforts to not only enhance future use of epigenetic inhibitors, but also translate similar approaches to other genetic-to-epigenetic pathways to control cancer growth. Our data demonstrate that the combined inhibition of the G2/M regulator, Aurora A, and the H3K9Me pathway is synergistic to inhibit PDAC growth. By inducing cell cycle arrest through inhibition of AURKA, the mitotic machinery is exposed longer to the H3K9Me pathway, which is well known to regulate centromere structure, triggering a cytotoxic mechanism that involves perturbation of normal mitotic progression to ultimately end in mitotic catastrophe, an attractive outcome in oncology. Inhibition of the H3K9 pathway, specifically in mitosis, offers a unique therapeutic approach not characteristically considered when utilizing epigenetic agents, which are generally applied in the context of modulating gene expression during interphase. My long-term research goals are broadly aligned with studying the regulation of histone methyl transferase complexes via similar signals that dictate the histone code and how those signals affect protein-protein interactions and function, as well as the type of dynamics (transient vs inherited) underlying the consequences of epigenetic targeting. Thus, we remain passionate about discovering molecular interactions and complex dynamics involved in epigenetic mechanisms triggered in response to cellular signals within the context of normal cell biology and pathophysiology and applying this knowledge to develop better therapeutic strategies in cancer.