All available projects are listed and described here, including the tasks for the internship. Applications can only be submitted through the application portal. Please do not submit your application until you have selected your preferred project.

Prof. Dr. Sabine Steffens

Institute for Diabetes and Cancer

Cardiovascular Disease Comorbidities

Project Description 

Epitranscriptomic regulation of cardiomyocyte stress adaptation by m6A RNA modifications

Cardiomyocytes adapt to physiological and pathological stress — including conditions such as diabetes — through tightly controlled gene-regulatory mechanisms. Small non-coding RNAs, particularly microRNAs (miRNAs), play important roles in post-transcriptional regulation during cardiac remodeling. Increasing evidence suggests that epitranscriptomic RNA modifications, including N6-methyladenosine (m6A) modifications affecting RNAs and miRNAs, may influence these regulatory pathways, yet their functional contribution to cardiac stress adaptation remains incompletely understood. Emerging observations from our laboratory indicate that cardiac stress signals can alter RNA modification patterns in stem cell-derived human cardiomyocytes, potentially shaping downstream gene-regulatory responses relevant for cardiac adaptation. This internship project aims to explore how stress-associated m6A RNA modifications contribute to cardiomyocyte adaptive responses. The work will focus on assessing RNA modification dynamics in stressed cardiomyocytes and examining their functional relevance for cellular remodeling processes. The project will provide general insight into epitranscriptomic regulatory mechanisms involved in cardiac stress adaptation.

Under close supervision, the intern will:
• Culture and maintain human stem cell-derived cardiomyocytes and apply controlled stress conditions
• Apply molecular biology techniques to assess m6A RNA modification status and generegulatory responses
• Perform functional assays to evaluate cellular adaptation processes
• Analyze, interpret, and visualize experimental data
• Gain experience in experimental design, data interpretation, and scientific communication

The intern will receive training in modern molecular and cellular biology techniques, participate in 
lab discussions, and contribute to ongoing research activities.

Dr. Siegfried Ussar

Helmholtz Diabetes Center

Adipocytes & Metabolism (ADM)

Project Description:

Validation and Characterization of Insulin Binding Aptamer-Based Diagnostics

Insulin is the central hormone regulating systemic glucose homeostasis, and its cellular content is a key marker of pancreatic β-cell function. Current methods to measure insulin levels and spatial distribution rely on highly specific antibodies used in ELISA and immunofluorescence 
assays. While effective, antibody-based diagnostics can be costly and may limit broader or continuous monitoring applications.
In this project, we explore DNA aptamers as a low-cost and highly selective alternative to antibodies. DNA aptamers are short, single-stranded oligonucleotides that can be generated in standard biology laboratories and bind target molecules with high affinity while being significantly 
smaller than antibodies. 

The aim of the project is to validate pre-selected insulin-binding aptamers and assess their suitability for use in ELISA-based assays and novel aptamer-based staining protocols. The intern will be embedded within our aptamer research group and gain hands-on experience with 
immunofluorescence staining, flow cytometry, and biochemical and cell biological assays to evaluate aptamer selectivity toward human and murine insulin and to determine binding affinities. Successful completion of the project will contribute to the development of a sensitive, low-cost insulin detection platform and may provide a foundation for future continuous or implantable insulin monitoring technologies.

Dr. Mauricio Berriel Diaz

Institute for Diabetes and Cancer

Division Metabolism and Cancer

Project Description

Functional Characterization of Tumor-Derived Mediators in Cancer Cachexia

Cancer cachexia is a multifactorial syndrome characterized by involuntary weight loss, reduced muscle strength, and atrophy, driven by metabolic dysregulation and anorexia induced by cancer. This systemic disorder affects multiple organs, significantly impairing the quality of life and prognosis of cancer patients. While significant progress has been made in understanding its pathomechanisms, key aspects remain to be fully elucidated, and effective treatment strategies are still needed. Despite the multifactorial nature of cancer cachexia, in which tumor-host metabolic interactions play a key role, tumor-secreted mediators are pivotal in initiating the wasting process. Although some phase II clinical trials target known cachexia mediators, these factors may be central only 
in a subset of patients, suggesting a certain degree of heterogeneity in the composition of factors driving cachexia development. This underscores the critical need to identify and functionally characterize novel tumor-derived mediators.

To this end, we employed innovative quantitative secretome analysis method combining click chemistry, pulsed stable isotope amino acid labeling and mass-spectrometry detection. This technology allowed us to selectively enrich and quantify secreted proteins from cell lines under optimal culture conditions (i.e. in the presence of serum), thereby identifying proteins differentially secreted between the well-established cachexia-inducing cell line Colon 26 (C26) and noninducing MC38 colon carcinoma cells. In this project, we aim to test and characterize the role of these candidate proteins in cancer cachexia using in vitro models, with the ultimate goal of identifying new potential mediators of cachexia and therapeutic targets for treatment.

Specifically, we will: a) characterize the expression and secretion of these proteins across a panel of cancer cell lines; b) perform gain- and loss-of-function experiments, including overexpression in non-cachexia-inducing cells and knockdown in cachexia-inducing cells; and c) investigate their mechanisms of action, potentially using pharmacological approaches to inhibit their function. This strategy will facilitate the pre-selection of potential tumor-derived mediators of cancer cachexia for further in vivo analyses. Ultimately, this approach holds promise for developing targeted treatments to mitigate muscle wasting, thereby alleviating the devastating impact of cancer cachexia and improving clinical outcomes for cancer patients.