About

Henk De Feyter, PhD, is an Associate Professor of Radiology and Biomedical Imaging at Yale School of Medicine. His research focuses on exploring biomarkers, tumor metabolism, and magnetic resonance spectroscopy, with particular interest in metabolic networks and pathways. His work involves the development and validation of deuterium metabolic imaging (DMI) for measuring cerebral metabolic rates of glucose, as well as metabolic imaging of brain tumors using deuterium and other advanced MRI techniques. De Feyter's contributions include establishing robust methods for deuterium abundance determination in water, and applying metabolic imaging to study brain tumor characterization, glucose consumption, and metabolic disorders. His research aims to advance noninvasive imaging tools for understanding tumor biology and brain metabolism, with ongoing investigations into the clinical translation of these techniques for diagnosing and monitoring brain tumors and metabolic conditions.

Research topics

• Biochemistry
• Cancer research
• Medicine
• Biology
• Nuclear medicine
• Endocrinology
• Internal medicine
• Pathology
• Chemistry

Selected publications

• Preclinical evaluation of a brain penetrant PARP PET imaging probe in rat glioblastoma and nonhuman primates

  European Journal of Nuclear Medicine and Molecular Imaging · 2023 · 15 citations

  • Nuclear medicine
  • Medicine
  • Pathology
  DOI

• Medulloblastoma uses GABA transaminase to survive in the cerebrospinal fluid microenvironment and promote leptomeningeal dissemination

  Cell Reports · 2021 · 55 citations

  • Biology
  • Endocrinology
  • Internal medicine

  Medulloblastoma (MB) is a malignant pediatric brain tumor arising in the cerebellum. Although abnormal GABAergic receptor activation has been described in MB, studies have not yet elucidated the contribution of receptor-independent GABA metabolism to MB pathogenesis. We find primary MB tumors globally display decreased expression of GABA transaminase (ABAT), the protein responsible for GABA metabolism, compared with normal cerebellum. However, less aggressive WNT and SHH subtypes express higher ABAT levels compared with metastatic G3 and G4 tumors. We show that elevated ABAT expression results in increased GABA catabolism, decreased tumor cell proliferation, and induction of metabolic and histone characteristics mirroring GABAergic neurons. Our studies suggest ABAT expression fluctuates depending on metabolite changes in the tumor microenvironment, with nutrient-poor conditions upregulating ABAT expression. We find metastatic MB cells require ABAT to maintain viability in the metabolite-scarce cerebrospinal fluid by using GABA as an energy source substitute, thereby facilitating leptomeningeal metastasis formation.

  DOI

Frequent coauthors

• Robin de Graaf

  19 shared

• Scott McIntyre

  Resonance Research (United States)

  8 shared

• Monique Thomas

  8 shared

• Chathura Kumaragamage

  8 shared

• Krista Fowles

  Yale University

  7 shared

• Jim Ropchan

  Yale University

  7 shared

• Zachary Corbin

  7 shared

• Richard E. Carson

  7 shared

Education

• PhD, Biomedical Engineering

  Technische Universiteit Eindhoven

  2007

• Ms., Bewegingswetenschappen

  Maastricht University Faculty of Health Medicine and Life Sciences

  2002

• Ms., DEPARTMENT OF PHYSICAL THERAPY AND MOTOR REHABILITATION

  Ghent University

  1999

Similar researchers at Yale University

• Mark Gersteinh-217
• Liangbing Huh-172
• Akiko Iwasakih-145
• Alan Kazdinh-142
• Douglas L. Rothmanh-125