Identification of epigenetic mechanisms contributing to glioma drug resistance


Our understanding of cancer treatment has increased over the years and as a result the personalized treatments became available. However, for patients with aggressive brain tumors, glioblastomas, the prognosis has not changed much and the average survival is still shorter than 15 months. This is associated with the high resistance of the tumor to the treatment. Systematic analyses confirmed that the treatment resistance is associated with the glioblastoma cellular heterogeneity. The presence of the non-differentiated cell subpopulation called ‘cancer stem cells’ is one of the major obstacles in a successful therapy. Although it was shown that epigenetic regulation is crucial for maintenance of a non-differentiated state, up to date, there is no publicly available data on association of glioblastoma stem-like cells chromatin characteristics with the self-renewal and drug resistance. We hypothesize that a chromatin state regulating ’stemness’ of tumor cells will extend understanding of brain tumor pathobiology and trigger development of new therapeutic approaches. We propose a comprehensive epigenetic analysis of the glioblastoma stem-like cells which may contribute to the treatment resistance. The main goal of this project is to provide original and important contribution to understanding the epigenetic mechanisms in glioma stem-like cells underlying glioma recurrence and drug resistance. This will be achieved by an innovative approach combining computational and statistical methods with resources provided by precisely designed experiments and data available through public repositories. Direct analysis of the chromatin landscape in glioblastoma stem-like cells will provide insights into specific epigenetic regulatory networks involved in the glioblastoma recurrence and drug resistance.


Work in progress.


Coming soon.


This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No 665778. The funding was granted within the POLONEZ program from the National Science Centre in Poland (2016/23/P/NZ2/04111).