Claus Storgaard Sørensen

The paper identifies an ERCC2 mutation-associated mutational signature in targeted panel sequencing data linked to nucleotide excision repair deficiency in bladder cancer and shows its clinical relevance.

This study identifies ZATT/ZNF451 as a key factor in resolving stalled TOP2 cleavage complexes without relying on TDP2, proteolysis, or DSB repair pathways.

This paper introduces CRISPR-PTM and CRISPR-VEIS to quantitatively analyze endogenous phosphosite effects on cellular fitness and signaling, showing Y19 as a novel inhibitory site in the WEE1-CDK1 pathway.

The paper identifies helicases as frequently mutated enzyme families in cancer, showing their role in genomic instability and DNA repair defects, with AQR as a novel hemizygous tumor suppressor.

This study identifies distinct roles of BRCA2's two DNA binding domains in DNA repair and replication fork stability using genetic and biochemical methods.

The paper identifies CAD-bound genes involved in both muscle cell differentiation and cancer-causing translocations, showing CAD-induced breaks are physiologic in differentiation and linked to oncogenic gene regulation.

The paper identifies a chromatin compaction threshold mediated by histone H4K20 methylation that limits DNA replication licensing in G1 phase to maintain genome integrity.