Publication Prize 2022

Three young scientists are honored with the publication prize 2022 for their outstanding publications which have arisen from funding on the part of the foundation and were published in 2021.

All of the next-generation scientists funded by EKFS within the medical/scientific funding lines First and Second Application, Else Kröner Memorial Fellowships and Else Kröner Advancement Programmes were able to submit entries for the prize. Each of the prizes is endowed with EUR 10,000 for use at the prizewinner’s personal discretion.

Prize winners 2022:

Janina Ohrndorf, Lina Welz, PD Dr. Konrad Aden

PD Dr. Konrad Aden, Department of Gastroenterology & Institute of Clinical Molecular Biology, University Hospital Schleswig Holstein, for his paper in Gastroenterolgy, 2022 Jan;162(1):223-237.e11. doi: 10.1053/j.gastro.2021.09.057. Epub 2021 Sep 30.
The publication arises from the project “Atg16l1-mediated autophagy as a critical instructor of DNA damage responses in intestinal inflammation and carcinogenesis” (EKFS first application line) and the Else Kröner Clinican Scientist Professorship “Deciphering the impact of amino acid metabolism on intestinal immunity and chronic inflammation”.

Project description:

IBD is a chronic relapsing inflammatory disorder of the gastrointestinal tract. Colitis-associated carcinogenesis (CAC) represent a major long-term complication of IBD. The underlying pathophysiological processes leading to CAC are poorly understood. Here the authors show that chronic inflammation directly instigates carcinogenesis by inhibiting ribonucleotide excision repair (RER), a specialized DNA repair mechanism aiming to delete faulty incorporated ribonucleotides into the double-stranded DNA. Using conditional knockout models of genes involved in RER and endoplasmic reticulum (ER) stress, the authors show that the interplay of disrupted ER-stress and RER critically drive epithelial carcinogenesis. These findings point towards transcription-associated mutagenesis as a novel pathophysiological principle of how chronic intestinal inflammation directs intestinal carcinogenesis.  

Here you can find further information.


Dr. Peter Siska

Dr. Peter Siska, Department of Internal Medicine III, University Hospital Regensburg, for his paper in The Journal of Clinical Investigation 2021 Nov 15;131(22):e148225.
The publication arises from the Else Kröner Research Schools for Physicians Regensburg - Interdisciplinary Translational Immuno-Oncology 2017. Spokespersons: Prof. Dr. Peter J. Oefner, Prof. Dr. Wolfgang Herr, Prof. Dr. Philipp Beckhove

Project description:

Severely ill COVID-19 patients show a dysregulated immune response; however, the mechanisms are insufficiently explored to date. In this publication, we studied immune cells such as T cells, monocytes and granulocytes in the acute phase and in the recovery phase of COVID-19.
The immune cells of severely ill COVID-19 patients showed an increased mass of mitochondria, the “power plants” of the cells. However, the mitochondria were also damaged and showed an impaired function, leading to production of toxic oxygen radicals. The decreased mitochondrial function correlated with high expression of the protein basigin on the surface of T cells.
Treatment of patients with the drug dexamethasone led to increased mitochondrial function, an improved metabolism and a decreased expression of basigin in T cells. This could be reproduced in vitro.


PD Dr. Dr. Sebastian Zundler and Dr. Tanja Müller discuss research data.

PD Dr. Dr. Sebastian Zundler, Department of Medicine 1, University Hospital Erlangen, for his paper in Gut 2021 Aug 30;gutjnl-2021-324868. doi: 10.1136/gutjnl-2021-324868.
The publication arises from the project “Differential effects of therapeutic anti-α4β7 blockade on homing of leukocyte subsets to the inflamed gut with special focus on effector and regulatory T cells” (EKFS first application line in 2017).

Project description:

The treatment of inflammatory bowel diseases (Crohn’s disease, ulcerative colitis) with the anti-α4β7 integrin antibody vedolizumab leads to a wide range of actual individual serum concentrations. Taking advantage of flow cytometry and functional analyses on material from a large patient cohort, single cell RNA sequencing and a post hoc analysis of phase III study data, we could show that specific anti-inflammatory (regulatory) T cells are “resistant” to vedolizumab in a certain exposure range and may thus counteract inflammation in the gut. These results suggest for the future that individual dosing to reach optimal serum drug levels may substantially increase the therapeutic effects of vedolizumab.