Philipp Jungk

I work on data-driven modeling of replication stress (RS), a disruption of DNA replication, and chromosomal instability (CIN), processes that lead to an abnormal number or structure of chromosomes. To this end, I developed a transcriptional signature that quantifies RS independently of cell proliferation, a frequent confounder in tumors linked to genome instability. Since CIN is a time-dependent process, I am developing methods to reconstruct its dynamics from omics data. Using single-cell sequencing (scRNA-seq), tumor heterogeneity can be resolved more precisely, allowing the inference of evolutionary trees with a pseudotemporal component. Because scRNA-seq is widely available and provides not only genomic but also functional information, I aim to use these data to investigate both the temporal evolution and the functional consequences of RS and CIN.