Amplification of the epidermal growth factor receptor (EGFR) gene is found in primary glioblastomas in up to 83% of cases, occurs almost exclusively in this tumour type among brain tumours and therefore appears to represent a late event in the context of glial tumour progression. Although the amplification of numerous other genes has been detected in glioblastomas, the EGFR gene is by far the most frequently affected by amplification in this tumour type. Amplification of the EGFR gene regularly results in overexpression of the EGFR mRNA and the receptor protein, leads to excessive stimulation of downstream signalling pathways and is associated with a more aggressive tumour phenotype and poorer clinical outcome.
A significant proportion of amplified EGFR genes are rearranged due to the specific loss of a DNA fragment encompassing exons 2-7 (EGFRvIII); this leads to a deletion of the gene sequence coding for the extracellular receptor domain. This specific deletion occurs in up to 58% of all glioblastomas and is by far the most common mutation of the EGFR gene. The specific deletion mutated receptor is constitutively (ligand-independent) activated and mediates increased tumourigenicity and apoptotic resistance. Quantitative and qualitative aspects therefore make both the overexpressed wild-type receptor and EGFRvIII potentially important targets for different therapeutic strategies.
The clinical-experimental armamentarium against EGFR in oncological therapy was recently expanded to include the quinazoline erlotinib, a selective and reversible inhibitor of the EGFR tyrosine kinase. As part of the current research project, the influence of differential gene expression on the biological effect of erlotinib on glioblastoma cell lines is being investigated in vitro. The aim of the analysis is to identify gene expression profiles that are associated with sensitivity or resistance of glioblastoma cells to erlotinib.

In recent decades, extensive findings have been made in the field of craniocerebral trauma. A distinction has been made between primary craniocerebral trauma, which is the result of the direct impact of force on the head with lacerations, fractures and brain contusions, and secondary craniocerebral trauma with subsequent cellular processes with brain swelling and brain cell death.
Secondary brain damage with cell-mediated cell death is the focus of experimental research in our working group. The disturbed communication between the supporting cells of the brain (glia) and the brain cells themselves is of interest to us. We work on our research approaches in collaboration with the Institute of Neurobiology at the University of Ulm (Head: Prof Wolf).
Clinically, the focus is on improving preventive approaches to avoid traumatic brain injury in childhood. To this end, epidemiological observations are carried out jointly on an interdisciplinary basis with the Department of Paediatrics, Section of Paediatric Surgery, Department of Trauma, Hand, Plastic and Reconstructive Surgery.
In addition, morphological-clinical examinations of severe craniocerebral trauma with injuries to the brain stem are carried out (Prof Woischneck, Landshut Hospital).

Neurosurgery at the University of Ulm uses two different hybrid operating theatre concepts at the Günzburg and Ulm sites. One is an intraoperative robotics-supported angiography, the Zeego® system, and the other is an intraoperative 1.5 Tesla high-field MRI, the Brainsuite®.
In both hybrid operating theatre environments, various research projects are being carried out to optimise intraoperative imaging, develop and evaluate new imaging methods and improve the workflow in the hybrid environment.
If you have any questions about the current projects, please contact us by e-mail:

Zeego Ulm: Prof Dr med Thomas Kapapa
Brainsuite Günzburg: Prof Dr med Ralph König

A spontaneous subarachnoid haemorrhage is a life-threatening bleed from a vessel at the base of the skull. In up to 85% of cases, the cause is a ruptured aneurysm. This is usually followed by a narrowing of the cerebral vessels (vasospasm) in the period 3 to 21 days after the haemorrhage. The exact cause of this is still unclear. In addition to further haemorrhage, vasospasm is a life-threatening complication in the course of treatment.
The molecular-genetic and cellular-biochemical background is the aim of our research into vasospasm. The aim here is to clearly demonstrate an inflammatory-immunological component and to discover possibilities for intervention. mRNA and DNA-based communication pathways are being investigated as well as cell communication by means of cytokines and proteases. We are investigating these approaches on an interdisciplinary basis with the Section of Experimental Anaesthesia and the Department of Neurology.
Cognition is one of the most valuable functions of the brain. It is often impaired after a subarachnoid haemorrhage and prevents smooth reintegration into everyday life. We focus on the cause of these cognitive disorders and their precise characterisation.