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cells; 2) Model AML plasticity at the single-cell level; 3) Propose candidate therapeutic targets for in vivo validation. The PhD student will be embedded in a collaborative and supportive team, working
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Malignancies: From Mechanisms to Therapies”. In this CRC we will focus on myeloid malignancies as a model to dissect the various molecular mechanisms that enable and regulate cancer cell plasticity in AML. Our
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“Cellular Plasticity in Myeloid Malignancies: From Mechanisms to Therapies”. In this CRC we will focus on myeloid malignancies as a model to dissect the various molecular mechanisms that enable and regulate
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xenograft (PDX) models. To this end, the candidate will have direct access to cutting-edge mass spectrometry and advanced bioinformatics infrastructure. The project is part of the collaborative research
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Great interest in pre-clinical in vivo models Ideally initial experience with Bioinformatics experience, especially in R What we offer Goal-oriented, individual training and development opportunities
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“Cellular Plasticity in Myeloid Malignancies: From Mechanisms to Therapies”. In this CRC we will focus on myeloid malignancies as a model to dissect the various molecular mechanisms that enable and regulate
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of the synthetic peptide in chronic and acute heart failure animal models. The therapeutic peptide is derived from the protein S100A1, which plays a central role in maintaining normal heart function. The synthetic
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adults, characterised by severe genomic instability and a lack of targeted therapies. Using cutting-edge methods and unique primary patient-derived cell models, this project will seek to understand
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of the anaphase-promoting complex (APC/C) and the degradation of cyclin B1. If cyclin B1 levels fall below a critical threshold, cells undergo mitotic slippage, entering G1 without proper chromosome segregation