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Pharmacology and Toxicology
Antje Schaefer, PhD

Antje Schaefer, PhD

Assistant Professor

Locations

  • Pharmacology & Toxicology
    Basic Science Building
    Office: BSB-B6815; Lab: BSB-B6710

Contact Information

Education

PhD, Structural Biochemistry, Max-Planck-Institute for Molecular Physiology, Germany

Biography

Dr. Antje Schaefer joined the Department of Pharmacology & Toxicology at the Medical College of Wisconsin as an assistant professor in September 2024. Her research program focuses on the mechanisms that drive gastric and pancreatic cancer growth and therapy resistance, with the goal of defining novel, target-based therapeutic strategies for both lethal cancers. Visit Dr. Schaefer's lab website for additional information.

Prior to joining MCW, Dr. Schaefer was a research assistant professor with Dr. Channing Der at the Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill (UNC). She identified that the two most common mutations in the RHOA GTPase in gastric cancer are oncogenic cancer drivers and defined novel therapeutic targets to improve treatment of gastric cancer patients. She also studied the role of RHO GTPase-dependent cell plasticity in driving therapy resistance in RAS-mutant pancreatic, colorectal and head-and-neck-cancers and determined new strategies for combination therapies.

Dr. Schaefer pursued her PhD in RHO and RAS GTPase structure and biochemistry in the lab of Dr. Alfred Wittinghofer at the Max-Planck-Institute for Molecular Physiology in Dortmund, Germany. As a graduate student, she was recognized as a Minerva FemmeNet Program member of the Max-Planck Society. Dr. Schaefer conducted her postdoctoral training with Dr. Peter Hordijk at the Sanquin Blood Institute, Academic Medical Center Amsterdam, The Netherlands. She identified that leukocytes are recruited by an RHO-dependent stiffness gradient across the surface of the endothelial cells to permissive sites where they migrate from the blood vessel into the tissue. For her work, Dr. Schaefer was awarded the Sanquin Science Award, a Sanquin Blood Foundation Research Grant and she was a finalist of the Young Investigator Award from the German Society of Microcirculation and Vascular Biology.

Research Experience

  • Carcinoma, Pancreatic Ductal
  • Cell Plasticity
  • Drug Screening Assays, Antitumor
  • Organoids
  • ras Proteins
  • rho GTP-Binding Proteins
  • Stomach Neoplasms

Research Interests

  • Gastric and pancreatic cancer
  • RHO and RAS GTPases
  • Cancer drug resistance mechanisms
  • Cell plasticity

RAS GTPases (e.g., KRAS) and the similar RHO (RAS homologous) GTPases (e.g., RHOA) are key signaling proteins that regulate a variety of different cellular functions and, when dysregulated, drive pathological processes including cancer as well as developmental and neurological disorders. Four decades ago, mutationally activated RAS genes encoding KRAS, HRAS and NRAS were discovered in cancer and now comprise one of the most frequently mutated oncogene family. By contrast, the cancer-associated functions of RHO GTPases such as RHOA are poorly understood. Only ten years ago, mutations in RHO GTPases and fusion genes of RHO-regulating protein were identified in tumor sequencing studies. Unexpectedly, the cancer-inducing genetic mechanisms (e.g., localization of the mutational hotspots) between RHO and RAS proteins are strikingly different - despite their high similarity in sequence and structure. Thus, extrapolations from the key cancer driver RAS are of limited value. Consequently, RHO-driven cancers such as gastric cancer as well as certain hematopoietic and lymphoid cancers are poorly defined and highly lethal due to the lack of effective therapies. In addition, RHO GTPases play also a critical, yet poorly understood role in the mechanisms that drive treatment resistance in RAS-mutant cancers and, thus, limiting therapy success in patients.

Our research program addresses the following current challenges in the research field:

  1. Dissect the molecular mechanisms by which aberrant RHOA function, induced either by RHOA mutations or RhoGAP fusion genes, drive gastric cancer growth and therapy resistance.
  2. Define the molecular mechanisms by which RHO GTPases modulate treatment resistance in KRAS-dependent pancreatic cancer.

Our overall goal is to discover novel therapeutic vulnerabilities in order to develop better, targeted therapies for these lethal cancers. Our lab uses a multidisciplinary approach including advanced microscopy, functional genomics and proteomics, cancer drug pharmacology, structural biochemistry, patient-derived cell lines and organoids, and mouse models.

Publications

Publications of Antje Schaefer PhD from the Faculty Collaboration Database

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