Munich, Bavaria, Germany
Resident physician (PGY-1) in Neuroradiology at TUM Medical Center, beginning clinical training under the guidance of Professor Jan Kirschke. Recently graduated from LMU Munich with distinction in the German medical licensing examination (Ärztliche Prüfung, grade: very good), I bring a strong academic background and clinical experience from Munich, Cologne, and Boston. My interests lie at the intersection of neuroradiology, AI and translational research, supported by prior fellowships in immuno-oncology (FES, MSSO) and industry experience at Amgen Germany.
Diagnostic focus on imaging of brain and spine diseases using MRI, CT, and angiography, including advanced methods for visualizing brain function. Therapeutic focus on minimally invasive endovascular treatment of cerebrovascular diseases (e.g. ischemic stroke, intracranial hemorrhage) as well as interventional pain therapy of the spine.
Research Fellow at Imperial Brain & Spine under the guidance of Santhosh G. Thavarajasingam, contributing to neurosurgical research in collaboration with LMU Munich’s Department of Neurosurgery, with a focus on brain and spine disorders. Analyzed clinical data, contributing to publications that advanced understanding in neurosurgery.
In 1999, the group of Walczak et al. demonstrated for the first time that TRAIL can be used safely in vivo and induces apoptosis of cancer cells while not harming healthy cells, whereas FasL is highly toxic when used in the same way. This good tolerability and its selectivity made TRAIL a promising candidate for cancer therapy. However, clinical trials with dulanermin (AMG951), a non-tagged zinc-coordinated soluble homotrimeric c-terminal recombinant TRAIL, failed. TNF and FasL are known to be released from the plasma membrane by metalloproteinase-mediated cleavage by ADAM17 and ADAM10, respectively. Although soluble TRAIL can be detected at a concentration of 100 pg/mL in the plasma of a healthy adult, the cleaving protease has not yet been deciphered. It is known that only the membrane-bound FasL, but not its soluble cytokine, can induce apoptosis. Considering the similarities in the downstream signaling pathways of TRAIL and FasL, this may explain the clinical failure of dulanermin. Therefore, the cleavage of TRAIL needs to be elucidated.
As an intern in Medical Communications at Amgen, I worked within the hematology and oncology franchise to support the preparation of scientific summaries, slide decks, and congress reports. The role sat at the interface of clinical data and strategic communication, requiring both scientific accuracy and clarity for diverse audiences. It was an instructive early look at how the pharmaceutical industry translates research into medical practice.
The FES scholarship gave me the space to pursue translational research I cared most about: work that moved between the bench and the bedside, and that took seriously the gap between biological understanding and clinical outcomes. Across neuroradiology, cell death signaling, and oncological surgery, the common thread in my research was a focus on conditions where current treatment options remain insufficient. The FES fellowship was a concrete opportunity to build the interdisciplinary and international connections that this kind of work demands.