Benjamin Dekel, MD, PhD
Project Title
The role of extracellular vesicles in Ewing sarcoma progression and potential therapeutics
About the Investigator
Prof. Dekel’s academic journey is marked by excellence. He graduated with honors, earning his BSc and MD from the Technion, followed by a PhD from the Weizmann Institute. He completed a Pediatric Residency at Sheba, a Post-Doctoral fellowship in stem cell biology at Weizmann, and a Pediatric Nephrology Fellowship at Schneider Medical Center. As a visiting Professor at Stanford’s Institute of Stem Cell Biology, he expanded his expertise. Prof. Dekel has received prestigious awards, including the Youdim Prize for Cancer Research, and is a member of the American Society of Clinical Investigation and the Israeli National Academy of Science in Medicine.
About the Research
Cancer spreads not only through the growth of tumor cells, but through the messages those cells send to their surroundings. One of the most powerful ways tumors communicate is via extracellular vesicles (EVs)—tiny “messages in a bottle” released by cancer cells and delivered to nearby and distant tissues, where they can reprogram healthy cells, weaken blood vessel barriers, and prepare new sites for tumor growth. In Ewing sarcoma (EWS), a rare and aggressive childhood cancer, metastatic spread—most often to the lungs—is the leading cause of death, and current treatments are highly toxic yet largely ineffective once the disease has spread. Growing evidence suggests that EVs play a central role in this process by carrying pro-cancer messages that help tumors invade and metastasize. Prof. Dekel’s research aims to intercept these messages by understanding how EWS cells use EVs to communicate with support cells, blood vessels, and the immune system, and how disrupting this communication can slow or prevent metastasis. Building on this concept, the proposed research repurposes BACE1/2 inhibitors, drugs originally developed for Alzheimer’s disease, to block the release or function of these EV messages, with the goal of restraining tumor growth and spread while avoiding the severe toxicity of conventional therapies. Using patient-derived tumor models and in vivo studies, this work seeks to establish EVs as key drivers of metastasis and pave the way toward a new, less toxic treatment strategy for children with metastatic Ewing sarcoma.
