Bente Benedict

TL;DR: Using multiple in vivo mouse models of liver cancer, treatment with combined inhibition of of CDC7 and mTOR results in a marked reduction of tumour growth, indicating that exploiting an induced vulnerability could be an effective treatment for liver cancer.

TL;DR: It is proposed that active removal of cohesin allows cancer cells to overcome DNA replication stress and leads to oncogene-induced cohesion loss from newly synthesized sister chromatids that may contribute to genomic instability and likely represents a targetable cancer cell vulnerability.

TL;DR: It is shown that abrogation of the G1/S-checkpoint allowed cells to enter S-phase under growth-restricting conditions at the expense of severe replication stress manifesting as decelerated DNA replication, reduced origin firing and accumulation of DNA double-strand breaks.

TL;DR: Results show that depletion of FANCD2 acts as a chemo-sensitizing strategy in pHGG, and suggest that celastrol treatment stalls ongoing replication forks, causing sensitivity to DNA-crosslinking in FAN CD2-dependent glioma cells.

TL;DR: In this paper, the authors used integrated bioinformatics analyses and a non-biased CRISPR loss of function genetic screen to identify potential therapeutic targets for hepatocellular carcinoma (HCC) cells.