Péter Hauser

Biography

Péter Hauser is working as a professor at Semmelweis University

Research Interest

Normal cells among anaerobic conditions initiate glycolysis – in 1930 Warburg observed that tumour cells are able to do the same among aerobic conditions. This so-called “aerobic glycolysis” enables the immediate availability of macro molecules required for quick cell division. A similar phenomenon has also been observed in the rapidly dividing embryonic cells. One of the “driver” genes behind this process is GLUT1, which boosts the cell’s extra glucose intake required for the process and the HIF1a and HIF2a transcription factors responsible for the initiation of glycolysis through the regulation of several genes. The metabolic transformation of energy is in closely linked to the six distinct characteristics of the formation of malign tumours (oncogenic activation, turning off tumour suppressors, replicative immortality, apoptosis avoidance, neovascularisation, metastatisation) which implies that genes present in the aforementioned characteristics are the drivers of the process instead of genes independent of it. The basis of the study is the hypothesis that the driver mutations most frequently occurring in the signal transmission pathways determine what role aerobic glycosys and the citric acid cycle will have in the energy retention of the given tumour. Therefore, we apply a novel approach which involves the study of the genes linked to glycosys in clinical groups involving various mutations. Thus the subject of our studies are not glycosys/mitochondrial oxidation or mutation but the combination of the two. This project exceeds the previous descriptive analysis of bioinfomratics by enabling the identification of not only the changing genes, and by the more thorough understanding of the molecular basis of tumour progression through the study of anaerobic glycosys.