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The researchers found decreasing variations in the expression of a proteins called BAZ2A. The standard known function of the protein would be to suppress factories that create cellular proteins and therefore have an effect on the viability of cells, says Prof. Roland Eils, who prospects a extensive study group at both DKFZ and at Heidelberg University. However when we switched off BAZ2A in the cell lines of metastasizing prostate malignancy, their development was paradoxically slowed. Further research showed that higher degrees of BAZ2A increased particular malignant properties of prostate cancer tumor cells, including their capability and flexibility to invade encircling tissue. A detailed molecular evaluation of prostate tumor cells demonstrated that the overproduction of BAZ2A resulted in alterations in epigenetic patterns which in turn inhibited the experience of several cancer-suppressing genes.