My project focuses on uncovering and validating non-mutational mechanisms of resistance to ALK inhibitors in ALK-positive ALCL. While targeted therapies like ALK inhibitors have significantly improved patient outcomes, treatment resistance remains a major obstacle to long-term success.
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Turner lab has established a patient-derived xenograft (PDX) model of ALK-positive anaplastic large cell lymphoma (ALCL), which gave me access to fresh tumor samples.
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Today, I’m a proud Marie Skłodowska-Curie Fellow under the EU Horizon Europe program—a fellowship that supports my work and enables international collaboration.
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My name is Rebekka Salzmann, and I’m from Germany. During my Bachelor’s in Biology at the University of Hamburg, I became fascinated by the complex mechanisms that govern the small components of our bodies.
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My doctoral research focuses on drug-tolerant persister cells (DTPs) and drug resistance mechanisms in ALK+ anaplastic large cell lymphoma (ALCL) and other ALK+ malignancies, such as non-small cell lung cancer (NSCLC).
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As part of the FANTOM EU project, I spent two weeks at CBmed in Graz, working on image analysis within the field of spatial proteomics, which was recently named Method of the Year 2024.
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As a part of my PhD in Gerda Egger’s lab, within the Fantom network, I contributed to a recently published paper in Leukemia entitled “HDAC1 acts as a tumor suppressor in ALK-positive anaplastic large cell lymphoma: implications for HDAC inhibitor therapy”.
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Currently, risk stratification for pediatric Hodgkin lymphoma is based on clinical factors such as stage, bulk, and systemic symptoms. Novel minimally invasive biomarkers could enhance both prognosis and treatment strategies.
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