Brain Tumor Translational Targets (B067)

Figure 1: Targeting GSCs to achieve complete degeneration of glioblastoma

Figure 1: Targeting GSCs to achieve complete degeneration of glioblastoma; a) Currently, the resistance of GSCs to radio- and chemotherapy allows this rare subpopulation of cells to persist after GBM treatment. Patients relapse with an aggressive tumour enriched in GSCs. b) Targeting GSCs with additional therapeutics will deplete this resistant sub-population, allowing complete degeneration of the tumour.

The aim of our research is to discover new therapeutics for giloblastoma patients, focusing on a therapy-resistant sub-population of cells, known as cancer stem-like cells. Glioblastoma urgently calls for an improvement of therapy success, implying many opportunities for translational research. Its annual incidence varies from 5 to 7 per 100,000: with around 25,000 new cases being diagnosed in the European Union each year.

Due to its location, aggressiveness and diffuse growth pattern, glioblastoma therapy is tremendously challenging and no significant improvement in survival has been achieved over the past decade. Much evidence has been gathered in recent years to reveal a small sub-population of cancer cells that are capable of continuous self-renewal and can regenerate the tumor. These are known as cancer stem-like cells (CSCs). Glioblastoma stem-like cells (GSCs) have been suggested to be responsible for the current therapy resistance of glioblastoma (Figure 1). In this respect, much effort needs to be directed towards the targeting of GSCs, which should cause the tumor to lose its ability to generate new cells, ultimately leading to complete tumor degeneration.

In recent years, the advent of high-throughput next-generation sequencing technologies has led to a new era in the study of de novo mutations, helping to uncover disease precondition and mechanism. However, these informative analyses do not account for post-translational modifications that lead to oncogene activation or tumor suppressor gene inhibition.

High-throughput phenotypic screens as performed in our group have proven to resolve this issue, identifying new druggable therapeutic targets for glioblastoma. Ultimately, we aim to translate our findings and perform preclinical studies to assess the therapeutic efficiency of newly identified targets’ inhibitors for brain tumor patients.



Dr. Violaine Goidts
Head of Division
Tel.: +49-6221-42-4635



Prof. Dr. C. Herold-Mende (Department of Neurosurgery, University Clinic of Heidelberg (Germany))

Prof. Dr. G. Reifenberger (Institute of Neuropathology, University Clinic of Düsseldorf (Germany))

Prof. Dr. T.O. Larsen (Department of Systems Biology, Technical University of Denmark)

Prof. Dr. I. Nakano (Neurosurgery, Neurology, Cell Developmental and Integrative Biology, Biochemistry and Molecular Genetics, University of Alabama at Birmingham (USA))

Dr. A. Hjemeland (Department of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham (USA))

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