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Ulcerative colitis (UC) is an incurable chronic intestinal disease which can severely reduce the quality of life for those affected. Even though novel therapy options are available, a long-term remission (absence of symptoms and inflammation) cannot be achieved in a large proportion of UC patients. In this project modern sequencing technologies will be utilized to detect complex molecular signatures displaying spatial resolution (spatial multi-omics) in intestinal biopsy samples from UC patients receiving biological therapy.

Congenital disorders of glycosylation (CDG) are inborn errors of metabolism that lead to severe, potentially fatal multisystem diseases. The project studies how cellular damage occurs due to the lack of sialic acid. The effect of the sialic acid precursor molecule N-acetylmannosamine on sugar chains (glycans) and metabolic processes is being investigated in order to develop a therapy on a long-term basis. Due to the key role of hyposialylation in the case of diseases affecting the central nervous system, the knowledge gained can deepen the understanding of these frequent disorders.

Fibrotic remodeling processes that occur for example in systemic sclerosis are a common cause of morbidity and mortality in industrialized countries. The currently used models of fibrosis for therapeutic testing are based on mice or cultured fibroblasts, and thus reproduce the development and course of fibrotic diseases only to a limited extent. In the proposed project the scientists aim to establish complementary models of fibrosis using human cells with varying complexities and throughput capacities.

The junior research group is investigating mechanisms to improve therapeutic response rates following radiation therapy or combined radioimmunotherapy. At the same time, the team is researching the underlying mechanisms of the side effects of such combination therapies. In this experimental research project the scientists want to investigate the influence of hormonal mechanisms on the development of antitumor immune responses following radiation therapy, or the combination of radiation therapy with immune checkpoint blockade.

Despite the kidney’s tremendous capacity for renal functional reserve (RFR), acute kidney injury (AKI) often leads to chronic kidney disease (CKD). Over 850 million people are affected worldwide. There is a lack of medication potentially able to prevent or stop a deterioration of renal function following acute damage. Modern single-cell transcriptomic technologies bear the potential to fundamentally change our knowledge about disease processes at the cellular level. The project aims to elucidate cellular signatures (“endophenotypes”) of both successful and maladaptive/scarring repair.

The aim of the project is to establish a two-component treatment scheme for tumor therapy: On the one hand, the cell cycle is stopped by a tumor suppressor pulse activation. This protects normal cells while leaving tumor suppressor-mutant cancer cells vulnerable to DNA-damaging chemotherapeutic agents.

Inhibitiors of the adaptor protein Menin are evolving as a novel class of drugs in acute leukemia with the potential to become the first targeted therapeutics that promise a curative treatment. Despite impressive clinical activity in phase-1 clinical trials, disease persistence has been observed leading to resistance development in some patients. In this project, the team will characterize molecular signatures underlying disease persistence during Menin-inhibition and investigate how specific epigenetic regulators re-program leukemia cells towards a “persister-state”.

Single-sided deafness reduces speech recognition in background noise, limits localisation of sound sources and can cause exhaustion, frustration, and social isolation.