• Use cell lines and mouse models to investigate the causal link between mitochondrial dysfunction and the pathophysiology of cancer
• Use molecular biology, biochemistry and imaging techniques to investigate molecular mechanisms
• Perform multiomics analyses (metabolic, proteomic and transcriptomic studies) and integrate these datasets to generate new hypotheses
• To accurately record and judiciously analyse, present, and report experimental data 
• Drive your own research project under direct supervision of the senior post docs and PI

• A completed Master’s degree in life sciences or related fields is mandatory
• Proficiency in written and spoken English is mandatory
• Evidence of great communication and team work skills, curiosity-driven science and excellent problem-solving skills
• Experience in animal tissue handling, cell culture or imaging is a plus
• Experience in systems/computational biology is plus
• A background in physiology, metabolism or cancer is a plus
• Proficiency in R studio or other programming language is desirable

• Everything but ordinary: You can expect a secure job in a challenging, innovative environment – including company pension schemes and regular working hours without business trips.
• Work-life balance: Whether full-time or part-time, with or without children – with numerous support options, we will find the right path together.
• Team spirit in R(h)ine culture: You will be warmly welcomed by an interdisciplinary team that values mutual respect and helpfulness.
• Strong perspectives: We offer extensive training opportunities – so you can continuously grow and set new goals.

CECAD is an inclusive, equal opportunity employer that offers attractive conditions and benefits commensurate with an international research organization with a very collegial and family-friendly work environment.
The Frezza laboratory (Christian Frezza Lab: Home) seeks to understand the contribution of dysregulated metabolism to age associated disorders, in particular focusing on cancer. A part of the lab is investigating how the loss of the mitochondrial enzyme and tumour suppressor Fumarate Hydratase causes renal cancer. Our work has multiple implications: (1) it will provide a mechanistic understanding of the role of metabolism and small molecule metabolites in human diseases; (2) it will generate experimental and computation tools to identify metabolic vulnerabilities that we can use as pharmacological targets for cancer therapy; (3) it will apply metabolomics and multi-omics analyses, to mouse and human models to identify metabolic markers of disease initiation for clinical application in early detection and for patient stratification.
The project of the successful candidate is part of the CRC1218 consortium (SFB1218) on "Mitochondrial regulation of cellular function".