AG Brandts

Prof. Christian Brandts, MD

University Hospital Frankfurt
Goethe University
Theodor-Stern-Kai 7
60590 Frankfurt

Phone:   +49 (0) 69 / 6301 - 87334 (office)
Fax:        +49 (0) 69 / 6301 - 83833
Email: brandts[at]




Christian Brandts, Principal Investigator
Shabnam Shaid, MD, Post-doctoral fellow, Laboratory coordinator
Ibrahim Polat, MD, Post-doctoral fellow
Sebastian Koschade, MD, Post-doctoral fellow
Fatima Baker, PhD student
Laura Meyer, PhD student
Marlyn Thölken, MTA
Lea Hermann, MD student
Susanna Hock, MD student


Our research group focusses on the role of two degradative pathways involved in cancer: autophagy and proteasomal degradation. We use a combination of biochemical, cellular and genetic models to investigate their role in acute leukemia and solid tumors.

Acute myeloid leukemia (AML) is a hierarchical disease of the bone marrow originating from a leukemia stem cell (LSC). A similar hierarchy is observed in solid tumors. Posttranslational modifications, such as phosphorylation and ubiquitination, are highly relevant during the process of malignant transformation. Functional ubiquitination is required at multiple steps of protein quality control. Autophagy is a fundamental degradation process to maintain cellular homeostasis by removing large protein complexes and damaged organelles, thereby serving as an essential cellular quality control system. Our laboratory is investigating how to target these degradation pathways to potentially develop novel therapies for cancer patients.

As part of the SFB1177 on Selective Autophagy, our research group has demonstrated that the process of selective autophagy plays an essential role in the development of leukemia. The targeted elimination of substrates with the help of autophagy receptors is critical for efficient leukemogenesis. The dynamic process of autophagic flux is highly active in AML blasts (including LSCs) compared to normal hematopoietic stem and progenitor cells.

How does autophagy prevent malignant transformation? How does autophagy support cancer cells to maintain their malignant phenotype? Can we use this knowledge to develop novel cancer therapies?

Our laboratory aims to answer these questions, in particular by identifying the underlying mechanism and investigating the therapeutic potential of targeting cancer cells by autophagy inhibition. Specifically, we are exploring the contribution of selective autophagy to cancer development and progression, as well as in treatment resistance. Our translational research laboratory makes use of genetic mouse models, proteomics, primary tumor material and clinical data, aiming at bringing results from the laboratory towards clinical trials.



We are always interested in applications from excellent