Chromosomal instability plays a crucial role in the progression of cancer: it shapes the properties of tumor cells and drives the development of therapy resistance. Scientists from the German Cancer Research Center (DKFZ), the Heidelberg Stem Cell Institute HI-STEM* and the European Molecular Biology Laboratory (EMBL) used state-of-the-art single-cell analysis methods to analyze the cellular heterogeneity of a specific form of acute myeloid leukemia. Their data show how genetic and non-genetic factors determine the functional heterogeneity of blood cancer cells and reveal new therapeutic targets.
In particular, under the selection pressure of cancer therapies, tumor cells undergo a veritable evolution to adapt to the changing conditions – and often escape the effects of therapy as a result. This evolution under therapeutic pressure is driven by a combination of genetic changes and non-genetic influences. Epigenetic modifications and changes in the transcriptome play a central role here, promoting the adaptation and activation of proliferation and survival programs.
